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Maternal exposure to polystyrene nanoplastics causes brain abnormalities in progeny
Abstract
As global plastic production continues to grow, microplastics released from a massive quantity of plastic wastes have become a critical environmental concern. These microplastic particles are found in a wide range of living organisms in a diverse array of ecosystems. In this study, we investigated the biological effects of polystyrene nanoplastic (PSNP) on development of the central nervous system using cultured neural stem cells (NSCs) and mice exposed to PSNP during developmental stages. Our study demonstrates that maternal administration of PSNP during gestation and lactating periods altered the functioning of NSCs, neural cell compositions, and brain histology in progeny. Similarly, PSNP-induced molecular and functional defects were also observed in cultured NSCs in vitro. Finally, we show that the abnormal brain development caused by exposure to high concentrations of PSNP results in neurophysiological and cognitive deficits in a gender-specific manner. Our data demonstrate the possibility that exposure to high amounts of PSNP may increase the risk of neurodevelopmental defects.
... The outcome encompasses a cumulative total of 973 mice, divided into 3 developmental stages embryonic, young, and adult. Among these, 17 studies specifically used male mice, three studies were performed on females, three studies involved both genders [28,30,34], and only one study did not specify the gender used [27]. ...
... Conversely, two studies have noticed a reduced level of a specific microglia marker Iba1 [29], and decreased GFAP levels [32]. Interestingly, despite these pronounced effects, the progeny didn't reveal any inflammatory alterations in response to PS-MP/NP exposure [27,28,30]. ...
... Although maternal exposure to 1 mg/L of PS-MP/NP did not induce significant neuroinflammation in the offspring [27,30]. Liver exposure at 10 mg/L and 1 mg/L of PS-NP during gestation significantly upregulated the expression of Il-6, TNf-a, and Il-1b in mice offspring [74]. ...
... These small particles can also induce oxidative stress, inflammation, increased apoptosis, and even malignancy in the female reproductive system (Fig. 1). The transfer of NPs from the mother's body to the fetus can accumulate in their various tissues, including the brain, liver, lungs, kidneys, and heart, causing disturbances in metabolism, reproductive function, immune function, neural development, and cognitive function [77,78]. Also, maternal exposure to MNPs can cause transgenerational toxicity and premature death in children [49,79]. ...
... The passage of NPs through the blood-placenta barrier (BPB) and their transfer via breast milk to offspring are the two main pathways through which offspring are exposed to nanoplastic particles [29,78], and the transfer of these materials through the placenta depends on their size [164]. Exposure of mother mice to NPs during pregnancy and lactation can cause deposition of these nanoparticles in the intestine, liver, brain, lungs, kidney, and heart tissues of the next generation mice and disrupts their immune system, nervous system, metabolism, and reproduction [29,77,78]. ...
... The passage of NPs through the blood-placenta barrier (BPB) and their transfer via breast milk to offspring are the two main pathways through which offspring are exposed to nanoplastic particles [29,78], and the transfer of these materials through the placenta depends on their size [164]. Exposure of mother mice to NPs during pregnancy and lactation can cause deposition of these nanoparticles in the intestine, liver, brain, lungs, kidney, and heart tissues of the next generation mice and disrupts their immune system, nervous system, metabolism, and reproduction [29,77,78]. ...
The female reproductive system can face serious disorders and show reproductive abnormalities under the influence of environmental pollutants. Microplastics (MPs) and nanoplastics (NPs) as emerging pollutants, by affecting different components of this system, may make female fertility a serious challenge. Animal studies have demonstrated that exposure to these substances weakens the function of ovaries and causes a decrease in ovarian reserve capacity. Also, continuous exposure to micro/nano plastics (MNPs) leads to increased levels of reactive oxygen species, induction of oxidative stress, inflammatory responses, apoptosis of granulosa cells, and reduction of the number of ovarian follicles. Furthermore, by interfering with the hypothalamic-pituitary-ovarian axis, these particles disturb the normal levels of ovarian androgens and endocrine balance and delay the growth of gonads. Exposure to MNPs can accelerate carcinogenesis in the female reproductive system in humans and animal models. Animal studies have determined that these particles can accumulate in the placenta, causing metabolic changes, disrupting the development of the fetus, and endangering the health of future generations. In humans, the presence of micro/nanoplastics in placenta tissue, infant feces, and breast milk has been reported. These particles can directly affect the health of the mother and fetus, increasing the risk of premature birth and other pregnancy complications. This review aims to outline the hazardous effects of micro/nano plastics on female reproductive health and fetal growth and discuss the results of animal experiments and human research focusing on cellular and molecular pathways.
... The Iimpact of Prenatal NPl/MPl Exposure on the Central NervousSystem and Retina of Mammalian Offspring (Table 1) Upon ingestion by mammals, NPl/MPl may exert local effects or enter the bloodstream to reach different organs and tissues [46,47]. Regarding maternal-fetal transfer, after maternal ingestion, NPl/MPl can penetrate the placenta and accumulate in fetal tissues, although the precise mechanisms by which MPl and NPl cross the placental barrier remain elusive [38][39][40]. In mice, prenatal and postnatal exposure to PS particles resulted in their accumulation in several brain regions, including the brainstem [48]. ...
... In pregnant and lactating dams, Jeong et al. [38] found that oral exposure of pregnant and lactating dams to PS-NPl resulted in a higher transfer of these particles to the brains of offspring through lactation than through the placenta prenatally. The authors [38] found that transcriptional expression of genes associated with neurogenic stem cell proliferation was reduced in the hippocampal region of offspring mice, accompanied by an imbalance in energy metabolism in neuroglial cells, upon oral exposure of pregnant and lactating mice to PS-NPl. ...
... In pregnant and lactating dams, Jeong et al. [38] found that oral exposure of pregnant and lactating dams to PS-NPl resulted in a higher transfer of these particles to the brains of offspring through lactation than through the placenta prenatally. The authors [38] found that transcriptional expression of genes associated with neurogenic stem cell proliferation was reduced in the hippocampal region of offspring mice, accompanied by an imbalance in energy metabolism in neuroglial cells, upon oral exposure of pregnant and lactating mice to PS-NPl. Prenatal and postpartum exposure to PS-NPl substantially reduced the thickness of the neuronal layer and corpus callosum in the CA3 region of the offspring. ...
The issue of environmental nanoplastic (NPl) particle and microplastic (MPl) particle pollution is becoming increasingly severe, significantly impacting ecosystems and biological health. Research shows that NPl/MPl can penetrate the placental barrier and enter the fetus, leading to transgenerational effects. This review integrates the existing literature on the effects of prenatal NPl/MPl exposure on mammalian offspring, focusing particularly on its negative impacts on the central nervous system, liver, intestinal health, reproductive function, and skeletal muscles. The vast majority of previous studies on prenatal NPl/MPl in mammals have used polystyrene material. Future research should explore the effects of other prenatal NPl/MPl materials on offspring to better reflect the realities of the human environment. It is also essential to investigate the potential harm and underlying mechanisms associated with prenatal NPl/MPl exposure to offspring in greater depth. This will aid in developing appropriate prevention and treatment strategies in the future.
... Furthermore, multiple factors impact the absorption and expulsion of MPs in the lungs, including hydrophobicity, surface charge, surface functionalization, surrounding protein coronas, particle size, and the various reactive groups present on the surface of MPs (Laganà et al., 2023;Yee et al., 2021). A study conducted by Jeong et al. (2022) used BEAS-2B human bronchial epithelial cells to assess the adverse impacts of PS-MPs. The study demonstrated that positively charged polystyrene microplastics (PS-MPs) exhibited cytotoxicity, enhanced ROS formation in BEAS-2B cells, and induced the expression as well as secretion of the pro-inflammatory cytokine IL-β in the animal model. ...
... The impact of MPs varies depending on their nature. In the case of PE-MPs, they have been found to cause anxiety and locomotor impairment in mice (Jeong et al., 2022). Research has also shown that fluorescently-labelled pristine PS-MPs induce behavioural changes and modifications in immunological markers in the liver and brain tissues of both young and elderly C57BL/6 J mice and have an age dependent impact (Gaspar et al., 2023). ...
Microplastics (MPs) have become a worldwide environmental concern that pose a threat to human health. An enormous increase in the manufacture and use of fossil-based plastics worldwide, coupled with improper waste management, causes plastic waste to deteriorate and produce MPs. MPs pose a severe health risk since they can infiltrate the body through a number of routes, including dermal contact, inhalation, and ingestion, eventually resulting in toxicity and a variety of disorders in humans. The presence of MPs has permeated the food chain, consequently intensifying the potential risk to human health. Moreover, the chemical components from the MPs can leach into the body, expanding their negative effects to trigger an immune response and induce oxidative stress reactions, genotoxicity, cancer, etc. Therefore, understanding the chemical composition of various synthetic plastics, which eventually transform into MPs and contribute to the onset of human disorders, is crucial. This chapter will also address the harmful impacts of MPs on several human organs and organ systems.
... Studies investigating the possible harmful effects of microplastics on reproduction at the cellular level and in animal models have increased recently. The first reports of microplastics found in human placenta and meconium were reported in 2021 [12,[16][17][18][19]. Chronic MP particle ingestion in mice can cause metabolic disorders, intestinal barrier failure, and dysbiosis of the gut microbiota [7]. ...
... Based on research on animals and in vitro cultures, there is growing proof that plastic particles are hazardous to fetuses and the placenta. According to studies, maternal exposure to microplastics during breastfeeding and pregnancy altered the neural cell compositions and the histology of the offspring's brains [16,18,20,21]. Studies have shown that exposure to MPs during pregnancy and the first few months of life may result in permanent alterations to the reproductive axis and central nervous system in the offspring of different species [16,21,22]. ...
Microplastic (MP) pollution is a growing global concern because of its potential to impair human health, particularly with regard to fetal development. However, the origins of prenatal MP exposure and its effects on fetal development have not been well studied. This study aimed to provide a systematic review of the literature regarding the impact of microplastics on pregnancy and fetal development.
PubMed, Embase, ScienceDirect, Web of Science, Scopus, and Google Scholar were searched from 2010 until March 2024. Original publications exploring the impact of microplastics on pregnancy and fetal development were included in the study. After selecting papers, two independent reviewers extracted data regarding study characteristics, microplastics identified, and reproductive impacts. The quality of studies was assessed using the Critical Appraisal Checklists for Studies created by the Joanna Briggs Institute (JBI). Twelve studies, including 234 subjects, were selected from a total of 2,809 citations for the final qualitative analysis. Articles were published between 2021 and 2024, and most were conducted in China. The results of the included studies confirmed the existence of microplastics with varying sizes (2.1 to 100 micrometers) in the placenta and the fetal body. Studies revealed correlations between lifestyle choices and the presence of microplastics in the placenta. They also reported correlations between the level of microplastics and diminished microbiome diversity, reduced birthweights, affected gestational age, and fetal growth and development. Microplastics may be detrimental to a developing fetus during pregnancy. Nonetheless, more thorough research is required to comprehend the impact of microplastic exposure on pregnancy and fetal development.
... Studies investigating the possible harmful effects of microplastics on reproduction at the cellular level and in animal models have increased recently. The first reports of microplastics found in human placenta and meconium were reported in 2021 [12,[16][17][18][19]. Chronic MP particle ingestion in mice can cause metabolic disorders, intestinal barrier failure, and dysbiosis of the gut microbiota [7]. ...
... Based on research on animals and in vitro cultures, there is growing proof that plastic particles are hazardous to fetuses and the placenta. According to studies, maternal exposure to microplastics during breastfeeding and pregnancy altered the neural cell compositions and the histology of the offspring's brains [16,18,20,21]. Studies have shown that exposure to MPs during pregnancy and the first few months of life may result in permanent alterations to the reproductive axis and central nervous system in the offspring of different species [16,21,22]. ...
Microplastic (MP) pollution is a growing global concern because of its potential to impair human health, particularly with regard to fetal development. However, the origins of prenatal MP exposure and its effects on fetal development have not been well studied. This study aimed to provide a systematic review of the literature regarding the impact of microplastics on pregnancy and fetal development. PubMed, Embase, ScienceDirect, Web of Science, Scopus, and Google Scholar were searched from 2010 until March 2024. Original publications exploring the impact of microplastics on pregnancy and fetal development were included in the study. After selecting papers, two independent reviewers extracted data regarding study characteristics, microplastics identified, and reproductive impacts. The quality of studies was assessed using the Critical Appraisal Checklists for Studies created by the Joanna Briggs Institute (JBI). Twelve studies, including 234 subjects, were selected from a total of 2,809 citations for the final qualitative analysis. Articles were published between 2021 and 2024, and most were conducted in China. The results of the included studies confirmed the existence of microplastics with varying sizes (2.1 to 100 micrometers) in the placenta and the fetal body. Studies revealed correlations between lifestyle choices and the presence of microplastics in the placenta. They also reported correlations between the level of microplastics and diminished microbiome diversity, reduced birthweights, affected gestational age, and fetal growth and development. Microplastics may be detrimental to a developing fetus during pregnancy. Nonetheless, more thorough research is required to comprehend the impact of microplastic exposure on pregnancy and fetal development.
... Research has increasingly focused on the health impacts of MPs on various organisms, with studies frequently utilizing model species like zebrafish (Danio rerio), mice (Mus musculus), and rats (Rattus norvegicus) [8]. Studies in mice have documented increased oxidative stress and decreased energy metabolism following MP exposure [9,10]. Multiple studies have demonstrated that MP exposure in animal models leads to significant reproductive disruptions, including decreased sperm quality, altered testosterone levels, and damage to testicular tissues [11][12][13][14][15][16][17]. ...
Aim: Microplastics (MPs), widespread environmental contaminants, pose a growing risk to livestock and other animals by potentially polluting their feed and ecosystems. This study aims to investigate the impact of MP exposure on oxidative stress, testicular function, and androgen receptor gene expression in mice, providing insights into the potential reproductive health risks for animals. Methods: Adult male mice were divided into three groups: a control group and two groups exposed to polystyrene microplastics (PS-MPs) at concentrations of 0.1 mg/0.5 mL and 0.2 mg/1 mL, respectively. We evaluated antioxidant enzyme levels (CAT, SOD, POD), reactive oxygen species (ROS) levels in testes, sperm count, viability, and motility, as well as histological changes in the testicular tissue. Furthermore, the gene expression levels of AR were assessed using qRT-PCR. Results: Exposure to PS-MPs led to a dose-dependent decrease in antioxidant enzyme levels and an increase in ROS levels in the testes. Similarly, sperm count, viability, and motility were significantly reduced in the PS-MPs treated groups. Histological examinations revealed a noticeable adverse effects on testicular development, with a marked reduction in germ cell populations. The analysis of gene expression showed significant downregulation of AR genes in mice exposed to PS-MPs, indicating the potential endocrine-disrupting effects of MP exposure. Conclusion: This study reveals that polystyrene MP exposure causes oxidative stress and reproductive damage in mice. These findings highlight the potential risks for livestock and other animals through contaminated feed, emphasizing the need for further research on microplastics' impact on animal health in agricultural ecosystems.
... Polystyrene NPs exposure altered cell membrane integrity and induced autophagy initiation and autophagosome production, along with mitochondrial damage, in human umbilical vein endothelial cells (HUVECs) [48,49]. It has been observed that maternal administration of polystyrene NPs in mice impaired progeny nervous system development and led to neurophysiological and cognitive deficits [50]. Tang et al. demonstrated that mice exposed to polystyrene NPs during gestation displayed lower birth weight and higher adult weight compared to non-NPs exposed mice [51]. ...
The escalation of plastic pollution represents a global environmental and health problem. Important toxic effects have been attributed to the increasing diffusion of microplastics (MPs) and nanoplastics (NPs) derived from the degradation of plastics. These particles have been ubiquitously observed in the environment, with humans being continuously exposed via ingestion, inhalation and skin contact. Nonetheless, the cellular homeostasis imbalance induced by micro- and nano- plastics (MNPs) in human health has been only recently shown, while most evidence and molecular mechanisms derived from studies in vitro and in vivo models. To date, the majority of available results testified the accumulation of MNPs in the cardiovascular, nervous, reproductive and digestive systems, and recently clear evidence about cardiovascular toxic effects of MNPs has been provided in humans. In this context, this review aims to provide a comprehensive update about the most recent studies reporting the effects of MNPs in different models, focusing on the available evidence in the main areas of study related to human health. Hopefully, this review will contribute to raise awareness about the toxicity and oxidative alteration exerted by MNPs, supporting the elaboration of new strategies to counteract plastic pandemics.
... This was also accompanied by decreased cell proliferation and elevated levels of pro-inflammatory factors [46]. Another study revealed that maternal exposure to PS-NP during gestation and lactation disrupted NSC functions and affected neural cell composition and brain histology in the offspring [123]. For a further review of MNP reproductive toxicity and its impact on female fertility and progeny health, we suggest the following articles [124,125]. ...
Microplastics and nanoplastics (MNPs) are ubiquitous environmental contaminants. Their prevalence, persistence, and increasing industrial production have led to questions about their long-term impact on human and animal health. This narrative review describes the effects of MNPs on oxidative stress, inflammation, and aging. Exposure to MNPs leads to increased production of reactive oxygen species (ROS) across multiple experimental models, including cell lines, organoids, and animal systems. ROS can cause damage to cellular macromolecules such as DNA, proteins, and lipids. Direct interaction between MNPs and immune cells or an indirect result of oxidative stress-mediated cellular damage may lead to increased production of pro-inflammatory cytokines throughout different MNP-exposure conditions. This inflammatory response is a common feature in the pathogenesis of neurodegenerative, cardiovascular, and other age-related diseases. MNPs also act as cell senescence inducers by promoting mitochondrial dysfunction, impairing autophagy, and activating DNA damage responses, exacerbating cellular aging altogether. Increased senescence of reproductive cells and transfer of MNPs/induced damages from parents to offspring in animals further corroborates the transgenerational health risks of the tiny particles. This review aims to provoke a deeper investigation into the notorious effects these pervasive particles may have on human well-being and longevity.
... After passing through the membrane, PS-NPs become stressors in various mammalian cells, increasing ROS levels, disrupting redox balance, and causing further antioxidant responses and autophagy [12]. Several studies have shown that the toxic effects of PS-NPs are related to mitochondrial dysfunction [13], endoplasmic reticulum stress [14], lysosomal stress [15] and DNA damage [16,17]. ...
Background:
Polystyrene nanoplastics (PS-NPs) are becoming increasingly prevalent in the environment with great advancements in plastic products, and their potential health hazard to animals has received much attention. Several studies have reported the toxicity of PS-NPs to various tissues and cells; however, there is a paucity of information about whether PS-NPs exposure can have toxic effects on mammalian oocytes, especially livestock. Herein, porcine oocytes were used as the model to investigate the potential effects of PS-NPs on mammalian oocytes.
Results:
The findings showed that different concentrations of PS-NPs (0, 25, 50 and 100 μg/mL) entering into porcine oocytes could induce mitochondrial stress, including a significant decrease in mitochondrial membrane potential (MMP), and the destruction of the balance of mitochondrial dynamic and micromorphology. Furthermore, there was a marked increase in reactive oxygen species (ROS), which led to oocyte lipid peroxidation (LPO). PS-NPs exposure induced abnormal intracellular iron overload, and subsequently increased the expression of transferrin receptor (TfRC), solute carrier family 7 member 11 (SLC7a11), and acyl-CoA synthetase long-chain family member 4 (ACSL4), which resulted in ferroptosis in oocytes. PS-NPs also induced oocyte maturation failure, cytoskeletal dysfunction and DNA damage. Cotreatment with 5 μmol/L ferrostatin-1 (Fer-1, an inhibitor of ferroptosis) alleviated the cellular toxicity associated with PS-NPs exposure during porcine oocyte maturation.
Conclusions:
In conclusion, PS-NPs caused ferroptosis in porcine oocytes by increasing oxidative stress and altering lipid metabolism, leading to the failure of oocyte maturation.
... Kim等人 [93] 曾对 4~8岁孩童体内双酚类化合物进行检测, 结果表明超过 微塑料在环境中的存在已经变得普遍, 特定尺寸 的微塑料能够突破皮肤屏障、胃肠道屏障而进入机体 血液循环 [94] . Dehghani等人 [95] [96] , 且能深入三维神经 球结构, 引发细胞的氧化应激, 造成细胞损伤 [97] 和神经 元细胞活性降低 [98] . [101] , 研究发现, 大脑皮质和边缘结构会对噪声产生应激作用, 抑制脑 [108] , 这些区域与 认知、记忆相关 [109] , 说明绿植暴露程度有利于提高儿 童的记忆能力和注意力, 原因是自然绿色环境减少了 级工作记忆增加了15.2%, ...
... Recently, alarm has been raised as their presence has also been recorded in tissue and biofluid samples from humans including placental tissue, breast milk and blood [13][14][15][16]. This concern has been further strengthened by findings from in vivo experiments on mammals, which have demonstrated that exposure to micro(nano)plastics can lead to abnormal brain development and cause traits similar to autism spectrum disorders [17][18][19], hinting that comparable effects might potentially be occurring in humans as a consequence of sustained microplastic exposure. ...
... Jeong investigated the biological effects of PS-NPs on the development of the central nervous system of mice using in vitro cultured neural stem cells [119]. The authors concluded that exposure to high concentrations of PS-NPs causes abnormalities in the infected animal's brain, resulting in cognitive problems and neurophysiological deficits. ...
Nanoplastics (NPs) have emerged as a concerning environmental pollutant due to their ubiquitous presence and potential adverse effects on human health. This review aims to elucidate the routes of NP contamination and their associated toxic effects on various systems within the human body. The inhalation of NPs presents a significant route of exposure, where particles can deposit deep within the respiratory tract, leading to potential respiratory health complications. Similarly, ingestion of NPs through contaminated food and water sources poses a risk to gastrointestinal and urinary tract health. Additionally, dermal permeation of NPs highlights another avenue for exposure, raising concerns about skin health. The potential toxic effects of micro(nano)plastics (MNPs) on human health span across multiple physiological systems. MNPs have been implicated in respiratory ailments, gastrointestinal disturbances, cardiovascular complications, blood abnormalities, compromised immune responses, neurological impairments, and reproductive dysfunctions. Understanding these toxic effects is crucial for developing strategies to mitigate NP exposure and protect human health. This review underscores the urgent need for interdisciplinary research efforts aimed at assessing NP toxicity comprehensively and implementing measures to reduce NP contamination in the environment.
... 18 Recent reports indicate that MPs have been found in human blood, 19 and similarly reports have shown that maternal exposure to polystyrene nanoplastics (PSNPs) increases the risk of neurodevelopmental defects in the offspring, leading to brain abnormalities in the offspring. 20 The environmental impacts of plastic particles are widespread and plastics can cause serious damage to ecosystems, with a large body of literature citing a variety of deleterious effects of plastics on ecosystems. 21,22 For example, MPs have affected aquatic organisms along the Caribbean coast of Colombia, leading to an increase in the activity of disease-causing microorganisms. ...
Microplastics and nanoplastics are emerging pollutants of concern in the aquatic environment that are causing increasing global environmental and human health problems. Although there has been extensive research on microplastics and nanoplastics, little has been said about the differences in their behavior in the aquatic environment, and many studies have considered them as the same class of hazardous materials; but in fact, microplastics and nanoplastics should be considered as two different types of environmentally hazardous materials. In this review, we propose that microplastics and nanoplastics behave in the aquatic environment in a size-dependent manner and should be distinguished. And we systematically analyzed the differences in the behavior of microplastics and nanoplastics in the aquatic environment in terms of five aspects: 1) distribution behavior; 2) adsorption behavior; 3) reaction with natural colloids; 4) aging and leaching behavior; 5) interaction with organisms. This paper has been written to draw academic attention to the different behaviors of microplastics and nanoplastics in the aquatic environment in order to distinguish between their effects on humans and the environment.
... It was discovered that foetal development limitation in mice was caused by maternal contact to PS-MPs and PS-NPs. According to research by Jeong and colleagues, maternally consumed PS-NPs entered the developing brains of future generation mice through feeding, where they produced neuronal malfunction and cognitive damage (Jeong et al., 2022). Similar to this, Fournier et al. discovered that following maternal pulmonary contact, PS was transferred from the maternal lung, passed the placenta to the fetal blood, and was then deposited in fetal organs such the hepatocytes, alveoli, renal tissue, myocardium, and neurons (Fournier et al., 2020). ...
The global COVID-19 pandemic has led to the enforcement of stringent measures to prevent the transmission of the severe lung illness it causes. However, there's growing concern about the environmental impact of these measures. Moreover, fine particulate matter, namely PM2.5 that harms lung health, especially after a pandemic, is a crucial contributor to the spread of the virus. In addition, microplastics and nano-plastics are released due to the breakdown of disposed face masks in nature, a process that is still poorly understood because of limited studies. Additionally, the spread of toxins from discarded face masks through air pollutants like PM2.5 and their detrimental effects on the ecosystem, including direct toxicity to human beings, the food chain, aquatic life, and companion animals, are taken into consideration. This review paper investigates analytical techniques and possible approaches to reduce the spread of discarded face masks and the contaminants they carry, while recognising the difficulties in tackling this intricate problem. By comprehending the interplay between face masks, COVID-19, and PM2.5, we may get a deeper knowledge of the repercussions and strive to reduce their detrimental impact on health and the environment by taking educated preventative steps. In conclusion, minimizing face masks' detrimental impact on human health, minimizing environmental pollution, and maintaining public health management depends on recognizing the possible hazards and taking necessary precautions.
Graphical Abstract
... This leads to neurophysiological and cognitive impairments. In male mice, this exposure also triggers testicular dysgenesis, subsequently influencing their fertility [30,31]. However, studies on the potential harmful effects of nanoplastic exposure during pregnancy on placental embryos are still limited. ...
Nanoplastics, created by the fragmentation of larger plastic debris, are a serious pollutant posing substantial environmental and health risks. Here, we developed a polystyrene nanoparticle (PS-NP) exposure model during mice pregnancy to explore their effects on embryonic development. We found that exposure to 30 nm PS-NPs during pregnancy resulted in reduced mice placental weight and abnormal embryonic development. Subsequently, our transcriptomic dissection unveiled differential expression in 102 genes under PS-NP exposure and the p38 MAPK pathway emerged as being significantly altered in KEGG pathway mapping. Our findings also included a reduction in the thickness of the trophoblastic layer in the placenta, diminished cell invasion capabilities, and an over-abundance of immature red cells in the blood vessels of the mice. In addition, we validated our findings through the human trophoblastic cell line, HTR-8/SVneo (HTR). PS-NPs induced a drop in the vitality and migration capacities of HTR cells and suppressed the p38 MAPK signaling pathway. This research highlights the embryotoxic effects of nanoplastics on mice, while the verification results from the HTR cells suggest that there could also be certain impacts on the human trophoblast layer, indicating a need for further exploration in this area.
... Additionally, 0.1 μm PS-NPs reduced the number of neural precursor cells and neuronal cells in a brain organoid model [30]. Both 50 nm and 500 nm PS-NPs decreased total cell numbers and neurite length in cultured hippocampal NSCs [31]. In the case of SVZ NSCs, 1 μm PS-MPs demonstrated greater cytotoxicity compared to 0.1 μm PS-NPs, while 2 μm PS-MPs exhibited the least effects. ...
Microplastics (MPs) and nanoplastics (NPs) are found in various environments such as aquatic, terrestrial, and aerial areas. Once ingested and inhaled, these tiny plastic debris damaged the digestive and respiratory organ systems in animals. In humans, the possible connection between MPs and various diseases such as lung diseases has been raised. Yet, the impact of MPs on the human nervous system has been unclear. Previous research using animals and cultured cells showed possible neurotoxicity of MPs and NPs. In this study, we used neural stem cells cultured from mouse subventricular zone to examine the effects of polystyrene (PS) NPs and MPs with sizes of 0.1 μm, 1 μm, and 2 μm on the cell proliferation and differentiation. We observed that only positively charged NPs and MPs, but not negatively charged ones, decreased cell viability and proliferation. These amine-modified NPs and MPs decreased both neurogenesis and oligodendrogenesis. Finally, fully differentiated neurons and oligodendrocytes were damaged and removed by the application of NPs and MPs. All these effects varied among different sizes of NPs and MPs, with the greatest effects from 1 μm and the least effects from 2 μm. These results clearly demonstrate the cytotoxicity and neurotoxicity of PS-NPs and MPs.
Nano-plastics (NPs), defined as particles smaller than 1 µm, have emerged as a significant environmental contaminant due to their potential ecological impacts. This study explores the size-dependent dynamics and tissue-specific distribution of polystyrene nano-plastics (PS-NPs) in Danio rerio exposed to PS-NPs at an environmentally relevant concentration of 1 μg/mL for 28 days, followed by a 17-day depuration period. PS-NPs of 20, 100, 200, and 500 nm were assessed in the intestine, liver, gills, muscle, and brain using transmission electron microscopy (TEM) and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Smaller PS-NPs (20 nm) showed the highest accumulation in the intestine, followed by the liver, and gills, due to their greater surface area and cellular penetration. In contrast, larger PS-NPs (500 nm) exhibited lower accumulation and clearance rates, especially in the brain, suggesting restricted passage through biological barriers. The intestine consistently had the highest concentrations in both accumulation and depuration, while the brain maintained the lowest across all nanoparticle sizes. During depuration, smaller particles cleared more quickly, whereas larger particles persisted. This study highlights the tissue-specific distribution and retention patterns of PS-NPs in D. rerio, providing insights into nanoparticle behavior in aquatic organisms and the need for long-term size-specific environmental risk assessments.
Keywords: Nano-plastics, D. rerio, bioaccumulation, depuration, tissue-specific distribution, Size-dependent dynamics.
A crescente preocupação com a poluição por microplásticos destaca a urgência em investigar seus efeitos na saúde humana, especialmente o acumulo na placenta e seus esfeitos. Estudos demonstram que as micro e nano partículas plásticas podem translocar-se pelo corpo, alcançando tecidos como a placenta, onde podem se acumular e impactar o desenvolvimento fetal. A exposição materna, como os de poliestireno, tem sido associada a anomalias cerebrais e restrição do crescimento fetal em modelos animais. Embora existam evidências sobre os efeitos agudos da exposição, há uma carência de estudos que explorem os impactos transgeracionais e em níveis de exposição ambientalmente relevantes. A necessidade de desenvolver métodos robustos para caracterizar essa exposição em humanos é imperativa, assim como a realização de investigações a longo prazo para entender quais as reais implicações na saúde das futuras gerações.
The widespread use of plastics has increased environmental pollution by micro- and nanoplastics (MNPs), especially polystyrene micro- and nanoplastics (PS-MNPs). These particles are persistent, bioaccumulative, and linked to endocrine-disrupting toxicity, posing risks to reproductive health. This review examines the effects of PS-MNPs on mammalian reproductive systems, focusing on oxidative stress, inflammation, and hormonal imbalances. A comprehensive search in the Web of Science Core Collection, following PRISMA 2020 guidelines, identified studies on the impact of PS-MNPs on mammalian fertility, including oogenesis, spermatogenesis, and folliculogenesis. An analysis of 194 publications revealed significant reproductive harm, such as reduced ovarian size, depleted follicular reserves, increased apoptosis in somatic cells, and disrupted estrous cycles in females, along with impaired sperm quality and hormonal imbalances in males. These effects were linked to endocrine disruption, oxidative stress, and inflammation, leading to cellular and molecular damage. Further research is urgently needed to understand PS-MNPs toxicity mechanisms, develop interventions, and assess long-term reproductive health impacts across generations, highlighting the need to address these challenges given the growing environmental exposure.
Plastics are versatile materials whose production and use are growing on a global scale. However, inadequate plastic waste management and its degradation result in the release of small particles, namely microplastics (MPs) and nanoplastics (NPs), which have adverse effects in physical, biological, and socioeconomic aspects. United Nations (UN) Sustainable Development Goal (SDG) 2 is related to ending hunger, promoting food security and nutrition, and achieving agricultural sustainability. MPs and NPs may affect the productivity and quality of agricultural products and contaminate foods and beverages from other sources, increasing health risks for human consumers. A systematic bibliographic review was conducted using StArt 3.4 and Excel software to identify gaps and recent advances in selected publications from 2022 and 2023 regarding the impacts of MPs and NPs to UN SDG 2. Then, 310 selected studies that discussed consequences to the agricultural soil, foods, drinking water, and beverages were summarized. The review addressed the recent advances and results regarding sources, occurrence, mobility, and effects of MPs and NPs on soil properties, nutrient cycling, productivity, and quality of agricultural soils. We also explored sources and MPs/NPs contamination of different types of foods, drinking water, and beverages. Hence, we highlighted the presence of plastic particles along the whole food production and consumption, which calls attention to the imperativeness of public policies and changes on plastic waste management cycle. We also reinforce the need for assessing MPs and NPs contamination considering local particularities, such as the climate, most common species, and feeding habits.
Graphical Abstract
Microplastics (MPs) have been detected in the atmospheric and the human respiratory system, indicating that the respiratory tract is a significant exposure route for MPs. However, the effect of inhaled MPs on cognitive function has not been adequately studied. Here, a C57BL/6 J mouse model of inhalation exposure to polystyrene MPs (PS‐MPs, 5 µm, 60 d) is established by intratracheal instillation. Interestingly, in vivo fluorescence imaging and transmission electron microscopy reveal that PS‐MPs do not accumulate in the brain. However, behavioral experiments shows that cognitive function of mice is impaired, accompanied by histopathological damage of lung and brain tissue. Transcriptomic studies in hippocampal and lung tissue have demonstrated key neuroplasticity factors as well as cognitive deficits linked to lung injury, respectively. Mechanistically, the lung‐brain axis plays a central role in PS‐MPs‐induced neurological damage, as demonstrated by pulmonary flora transplantation, lipopolysaccharide (LPS) intervention, and cell co‐culture experiments. Together, inhalation of PS‐MPs reduces cognitive function by altering the composition of pulmonary flora to produce more LPS and promoting M1 polarization of microglia, which provides new insights into the mechanism of nerve damage caused by inhaled MPs and also sheds new light on the prevention of neurotoxicity of environmental pollutants.
There are increasing concerns regarding the rapid expansion of polystyrene nanoplastics (PS-NPs), which could impact human health. Previous studies have shown that nanoplastics can be transferred from mothers to offspring through the placenta and breast milk, resulting in cognitive deficits in offspring. However, the neurotoxic effects of maternal exposure on offspring and its mechanisms remain unclear. In this study, PS-NPs (50 nm) were gavaged to female rats throughout gestation and lactation to establish an offspring exposure model to study the neurotoxicity and behavioral changes caused by PS-NPs on offspring. Neonatal rat hippocampal neuronal cells were used to investigate the pathways through which NPs induce neurodevelopmental toxicity in offspring rats, using iron inhibitors, autophagy inhibitors, reactive oxygen species (ROS) scroungers, P53 inhibitors, and NCOA4 inhibitors. We found that low PS-NPs dosages can cause ferroptosis in the hippocampus of the offspring, resulting in a decline in the cognitive, learning, and memory abilities of the offspring. PS-NPs induced NOCA4-mediated ferritinophagy and promoted ferroptosis by inciting ROS production to activate P53-mediated ferritinophagy. Furthermore, the levels of the antioxidant factors glutathione peroxidase 4 (GPX4) and glutathione (GSH), responsible for ferroptosis, were reduced. In summary, this study revealed that consumption of PS-NPs during gestation and lactation can cause ferroptosis and damage the hippocampus of offspring. Our results can serve as a basis for further research into the neurodevelopmental effects of nanoplastics in offspring.
Graphical Abstract
Background:
The widespread exposure to plastic products and the increasing number of individuals with cognitive impairments have imposed a heavy burden on society.
Objective:
This study aims to investigate the relationship between plastic product exposure in daily life and cognitive function in older Chinese individuals.
Methods:
Data were obtained from the 2023 Ningxia Older Psychological Health Cohort, comprising 4045 participants aged 60 and above. Cognitive function was assessed using the Mini-Mental State Examination scale. A population-based plastic exposure questionnaire was used to calculate plastic exposure scores (PES). Binary logistic regression was employed to analyze the relationship between PES and cognitive function, while restricted cubic splines were used to examine the dose-response relationship between PES and cognitive function. Latent profile analysis (LPA) was employed to explore the potential patterns of plastic exposure, and logistic regression was used to investigate the relationship between different exposure patterns and cognitive function. A linear regression model was utilized to investigate the relationship between PES and different dimensions of cognitive function.
Results:
Among the 4045 participants, 1915 individuals were assessed with mild cognitive impairment (MCI). After adjusting for all covariates, PES (OR = 1.04, 95% CI 1.02-1.06) was significantly associated with the risk of MCI and exhibited a dose-response relationship. LPA identified two potential categories of plastic exposure, with a higher risk of MCI observed in the group using plastic utensils.
Conclusions:
This study indicates a positive correlation between plastic exposure levels and MCI risk, particularly among individuals who frequently use plastic tableware.
Throughout history, animals have been a vital source of protein and energy and have been utilized in agriculture to produce food for human consumption. The increasing global demands for protein are being met through the increased production of meat, milk, eggs, and other food items, and is facilitated by the rapid pace of industrialization. However, the increase in food production and new technologies has led to the release of novel environmental pollutants, including microplastics (MPs). Currently, MPs are found in diverse ecosystems, exerting adverse effects in both terrestrial and aquatic organisms. While scientific evidence supports that MPs can harm aquatic organisms, recent studies have also begun to investigate the effects of MPs on terrestrial ecosystems, marking a significant shift from the traditional focus on aquatic environments. This chapter aims to synthesize current knowledge on the occurrence and distribution of MPs in food and their presence in aquatic and terrestrial animals, in addition to discussing the potential consequences for human health. Evidence supports that plastic mulching and compost are prominent sources of MPs in agricultural fields, whereas irrigation channels act as vital sources of MP contamination in aquaculture systems. A high abundance of MPs has been found in soil-dwelling worms, livestock, companion animals, and wild animals. In Africa, the north Tunisian lagoons of Bizerte, Ghar El Mehl and Lake Victoria are prominent areas of MP contamination. In Asia, China contributes the highest abundance of MPs to the environment. Exposure to MPs cause oxidative stress, immunotoxicity, neurotoxicity, reproductive impairment, and endocrine disruption in both terrestrial and aquatic animals. Current evidence suggests the need for further investigation into the specific sources of MP exposure in animals and the routes through which it enters the human body. Legislators need to implement programs and collective actions to modify public behaviour and reduce MPs pollution in the natural environment.
The scale of plastic pollution boggles the mind. Nearly 400 megatons of virgin plastics are produced annually, with an environmental release rate of 80 percent; and plastic waste including micro- and nanoplastics are associated with a plethora of problems. The naturally evolved abilities of plastic-degrading and consuming microbes offer a starting point for generating sustainable and eco-centric solutions to plastic pollution. Here we developed an iterative discovery procedure coupling faster quasi-high-throughput polyethylene terephthalate (PET) dependent bioactivity screens with longer-term PET biodegradation assays to find small molecule and ionic boosters of PET consumption by the bacterium Piscinibacter sakaiensis. We discovered multiple hits supporting greater than 2-fold enhancement of PET biodegradation - with hits belonging to a small but heterogeneous set of compounds and mixtures, suggesting upregulation of PET consumption via multiple paths. This work has the potential to advance the creation of a fermentation-based process for solving PET plastic pollution.
Emerging contaminants (ECs) pollution has attracted global attention, and a large number of ECs spread in the environment, threatening the ecological environment and human health. Gut microbiota is the most complex microbial community, and its high sensitivity to ECs exposure has been widely concerned and reported by researchers. In fact, many studies have demonstrated that the gut microbiota is closely related to host health and is a toxic target of various environmental pollutants including ECs. This review evaluates the interaction of ECs (including persistent organic pollutants, antibiotics, microplastics and environmental endocrine disruptors) with the gut microbiota, and considers the possible harm of ECs to human health, finding that the gut microbiota may be involved in the regulation of various organ damage, endocrine disorders, embryotoxicity, and cancer development and other toxic processes caused by ECs exposure through related mechanisms such as the gut-liver axis, direct effects, and gut-brain axis. In short, we hope that more future studies will pay more attention to the relationship between ECs, gut microbiota and human health.
This book covers key areas of biological science. The contributions by the
authors include antioxidant properties, different antioxidant assays, thiobarbituric
acid reactive substances, malonic dialdehyde, lipid peroxidation, metabolomics,
nuclear magnetic resonance, mass spectrometry, time-of-flight, hydatid cyst
disease, echinococcosis, benzadazole, mebendazole, curcuma longa, traditional
medicine, bioavailability, piperine, liposomal encapsulation, microplastics,
polyamid content, breast milk, infant formula, ocean calcifiers, ocean
acidification, foraminifera, calcite compensation depth, climate change, carbon
sequestration, pteridophytes, natural habitats, in-vitro and ex-situ conservation,
economic importance, air purification, air pollution tolerance index, conservation
of environment, high efficiency particulate air filters, air pollution remedies, toxic
pollutants, continuously stirred tank reactor, non-gregarious locust pests,
predictive simulation, phytosanitary forecasting, species distribution models,
ecological niche models. This book contains various materials suitable for
students, researchers, and academicians in the fields of biological science.
Microplastics (MPs) are particles with a diameter of <5 mm. The disposal of plastic waste into the environment poses a significant and pressing issue concern globally. Growing worry has been expressed in recent years over the impact of MPs on both human health and the entire natural ecosystem. MPs impact the feeding and digestive capabilities of marine organisms, as well as hinder the development of plant roots and leaves. Numerous studies have shown that the majority of individuals consume substantial quantities of MPs either through their dietary intake or by inhaling them. MPs have been identified in various human biological samples, such as lungs, stool, placenta, sputum, breast milk, liver, and blood. MPs can cause various illnesses in humans, depending on how they enter the body. Healthy and sustainable ecosystems depend on the proper functioning of microbiota, however, MPs disrupt the balance of microbiota. Also, due to their high surface area compared to their volume and chemical characteristics, MPs act as pollutant absorbers in different environments. Multiple policies and initiatives exist at both the domestic and global levels to mitigate pollution caused by MPs. Various techniques are currently employed to remove MPs, such as biodegradation, filtration systems, incineration, landfill disposal, and recycling, among others. In this review, we will discuss the sources and types of MPs, the presence of MPs in different environments and food, the impact of MPs on human health and microbiota, mechanisms of pollutant adsorption on MPs, and the methods of removing MPs with algae and microbes.
Due to weather and working/operational conditions, plastic degradation produces toxic and non-biodegradable nano and microplastics (N/M-Ps, ranging from 10 nm to 5 mm), and over time these N/M-Ps have integrated with the human cycle through ingestion and inhalation. These N/M-Ps, as serious emerging pollutants, are causing considerable adverse health issues due to up-taken by the cells, tissue, and organs, including the brain. It has been proven that N/M-Ps can cross the blood-brain barrier (via olfactory and blood vessels) and affect the secretion of neuroinflammatory (cytokine and chemokine), transporters, and receptor markers. Neurotoxicity, neuroinflammation, and brain injury, which may result in such scenarios are a serious concern and may cause brain disorders. However, the related pathways and pathogenesis are not well-explored but are the focus of upcoming emerging research. Therefore, as a focus of this editorial, well-organized multidisciplinary research is required to explore associated pathways and pathogenesis, leading to brain mapping and nano-enabled therapeutics in acute and chronic N/M − Ps exposure.
Background
Plastic is everywhere. It is used in food packaging, storage containers, electronics, furniture, clothing, and common single-use disposable items. Microplastic and nanoplastic particulates are formed from bulk fragmentation and disintegration of plastic pollution. Plastic particulates have recently been detected in indoor air and remote atmospheric fallout. Due to their small size, microplastic and nanoplastic particulate in the atmosphere can be inhaled and may pose a risk for human health, specifically in susceptible populations. When inhaled, nanosized particles have been shown to translocate across pulmonary cell barriers to secondary organs, including the placenta. However, the potential for maternal-to-fetal translocation of nanosized-plastic particles and the impact of nanoplastic deposition or accumulation on fetal health remain unknown. In this study we investigated whether nanopolystyrene particles can cross the placental barrier and deposit in fetal tissues after maternal pulmonary exposure.
Results
Pregnant Sprague Dawley rats were exposed to 20 nm rhodamine-labeled nanopolystyrene beads (2.64 × 10 ¹⁴ particles) via intratracheal instillation on gestational day (GD) 19. Twenty-four hours later on GD 20, maternal and fetal tissues were evaluated using fluorescent optical imaging. Fetal tissues were fixed for particle visualization with hyperspectral microscopy. Using isolated placental perfusion, a known concentration of nanopolystyrene was injected into the uterine artery. Maternal and fetal effluents were collected for 180 min and assessed for polystyrene particle concentration. Twenty-four hours after maternal exposure, fetal and placental weights were significantly lower (7 and 8%, respectively) compared with controls. Nanopolystyrene particles were detected in the maternal lung, heart, and spleen. Polystyrene nanoparticles were also observed in the placenta, fetal liver, lungs, heart, kidney, and brain suggesting maternal lung-to-fetal tissue nanoparticle translocation in late stage pregnancy.
Conclusion
These studies confirm that maternal pulmonary exposure to nanopolystyrene results in the translocation of plastic particles to placental and fetal tissues and renders the fetoplacental unit vulnerable to adverse effects. These data are vital to the understanding of plastic particulate toxicology and the developmental origins of health and disease.
Aquatic environments are generally contaminated with nanoplastic material. As a result, molecular mechanisms for sensitive species like Daphnia are needed, given that mechanistic nanoplastic toxicity is largely unknown. Here, global transcriptome sequencing (RNA-Seq) was performed on D. pulex neonates to quantitatively measure the expression level of transcripts. A total of 208 differentially expressed genes (DEGs) were detected in response to nanoplastic exposure for 96 h, with 107 being up-regulated and 101 down-regulated. The gene functions and pathways for oxidative stress, immune defense, and glycometabolism were identified. In this study, D. pulex neonates provide some molecular insights into nanoplastic toxicity. However, more studies on DEGs are needed to better understand the underlying mechanisms that result as a response to nanoplastic toxicity in aquatic organisms.
Microplastics are particles smaller than five millimetres obtained from the degradation of plastic objects abandoned in the environment. Microplastics can move from the environment to living organisms and, in fact, they have been found in fishes and mammals.
Six human placentas, prospectively collected from consenting women with uneventful pregnancies, were analyzed by Raman Microspectroscopy to evaluate the presence of microparticles. Detected microparticles were characterized in terms of morphology and chemical composition.
12 microparticles, ranging from 5 to 10 γm in size, were found in 4 out of 6 placentas: 5 in the foetal side, 4 in the maternal side and 3 in the chorioamniotic membranes. All the analyzed microparticles were pigmented: three of them were identified as stained polypropylene, while for the other nine it was possible to identify only the pigments, which are all used for man-made coatings, paints and dyes.
Here we show, for the first time, the presence of microparticles and microplastics in human placenta. This sheds new light on the impact of plastic on human health. Microparticles and microplastics in the placenta, together with the endocrine disruptors transported by them, could have long-term effects on human health.
Although the fates of microplastics (0.1–5 mm in size) and nanoplastics (<100 nm) in marine environments are being increasingly well studied1,2, little is known about the behaviour of nanoplastics in terrestrial environments3–6, especially agricultural soils⁷. Previous studies have evaluated the consequences of nanoplastic accumulation in aquatic plants, but there is no direct evidence for the internalization of nanoplastics in terrestrial plants. Here, we show that both positively and negatively charged nanoplastics can accumulate in Arabidopsis thaliana. The aggregation promoted by the growth medium and root exudates limited the uptake of amino-modified polystyrene nanoplastics with positive surface charges. Thus, positively charged nanoplastics accumulated at relatively low levels in the root tips, but these nanoplastics induced a higher accumulation of reactive oxygen species and inhibited plant growth and seedling development more strongly than negatively charged sulfonic-acid-modified nanoplastics. By contrast, the negatively charged nanoplastics were observed frequently in the apoplast and xylem. Our findings provide direct evidence that nanoplastics can accumulate in plants, depending on their surface charge. Plant accumulation of nanoplastics can have both direct ecological effects and implications for agricultural sustainability and food safety.
Aquatic ecosystems are globally contaminated with microplastics (MP). However, comparative data on MP levels in freshwater systems is still scarce. Therefore, the aim of this study is to quantify MP abundance in water and sediment of the German river Elbe using visual, spectroscopic (Fourier-transform infrared spectroscopy) and thermo analytical (pyrolysis gas chromatography mass spectrometry) methods. Samples from eleven German sites along the German part of the Elbe were collected, both in water and sediment phase, in order to better understand MP sinks and transport mechanisms. MP concentrations differed between the water and sediment phase. Sediment concentrations (mean: 3,350,000 particles m⁻³, 125–5000 μm MP) were in average 600,000-fold higher than water concentrations (mean: 5.57 particles m⁻³, 150–5000 μm MP). The abundance varied between the sampling sites: In sediments, the abundance decreased in the course of the river while in water samples no such clear trend was observed. This may be explained by a barrage retaining sediments and tidal influence in the upstream parts of the river. Particle shape differed sitespecifically with one site having exceptionally high quantities of spheres, most probably due to industrial emissions of PS-DVB resin beads. Suspended MP consisted predominantly of polyethylene and polypropylene whereas sediments contained a higher diversity of polymer types. Determined MP concentrations correspond well to previous results from other European rivers. In a global context, MP levels in the Elbe relate to the lower (water) to middle section (sediment) of the global range of MP concentrations determined for rivers worldwide. This highlights that elevated MP levels are not only found in single countries or continents, but that MP pollution is an issue of global concern.
Drug-protein binding plays a key role in determining the pharmacokinetics of a drug. The distribution and protein binding ability of a drug changes over a lifetime, and are important considerations during pregnancy and lactation. Although proteins are a significant fraction in plasma composition, they also exist beyond the bloodstream and bind with drugs in the skin, tissues or organs. Protein binding influences the bioavailability and distribution of active compounds, and is a limiting factor in the passage of drugs across biological membranes and barriers: drugs are often unable to cross membranes mainly due to the high molecular mass of the drug-protein complex, thus resulting in the accumulation of the active compounds and a significant reduction of their pharmacological activity. This review describes the consequences of drug-protein binding on drug transport across physiological barriers, whose role is to allow the passage of essential substances—such as nutrients or oxygen, but not of xenobiotics. The placental barrier regulates passage of xenobiotics into a fetus and protects the unborn organism. The blood–brain barrier is the most important barrier in the entire organism and the skin separates the human body from the environment.
Microplastics have recently been detected in the atmosphere of urban, suburban, and even remote areas far away from source regions of microplastics, suggesting the potential long-distance atmospheric transport for microplastics. There still exist questions regarding the occurrence, fate, transport, and effect of atmospheric microplastics. These questions arise due to limited physical analysis and understanding of atmospheric microplastic pollution in conjunction with a lack of standardized sampling and identification methods. This paper reviews the current status of knowledge on atmospheric microplastics, the methods for sample collection, analysis and detection. We review and compare the methods used in the previous studies and provide recommendations for atmospheric microplastic sampling and measurement. Furthermore, we summarize the findings related to atmospheric microplastic characteristics, including abundance, size, shapes, colours, and polymer types. Microplastics occur in the atmosphere from urban to remote areas, with an abundance/deposition spanning 1–3 orders of magnitude across different sites. Fibres and fragments are the most frequently reported shapes and the types of plastic which generally aligns with world plastic demand. We conclude that atmospheric microplastics require further research and greater understanding to identify its global distributions and potential exposure to human health through further field sampling and implementation of standardized analytical protocols.
Research on microplastics in soils is still uncommon and the existing publications are often incomparable due to the use of different sampling, processing and analytical methods. Given the complex nature of soils, a suitable and efficient method for standardised microplastic analysis in the soil matrix has yet to be found. This paper proposes a critical review on the different published methods for sampling, extraction, purification and identification/quantification of microplastics in complex environmental matrices, with the main focus on their applicability for soil samples. While large microplastic particles can be manually sorted out and verified with chemical analysis, sample preparation for smaller microplastic analysis is usually more difficult. Of the analytical approaches proposed in literature, some are established, while others are a proof of principle and have not yet been applied to environmental samples. For the sake of development all approaches are discussed and assessed for their potential applicability for soil samples. So far, none of the published methods seems ideally suitable for the analysis of smaller microplastics in soil samples, but slight modifications and combinations of methods may prove promising and need to be explored.
Recently, research on the biological effects of nanoplastics has grown exponentially. However, studies on the effects of nanoplastics on freshwater organisms and the mechanisms of the biological effects of nanoplastics are limited. In this study, the content of reactive oxygen species (ROS), gene and protein expression in the MAPK-HIF-1/NFkB pathway, and antioxidant gene expressions and enzyme activities were measured in Daphnia pulex exposed to polystyrene nanoplastic. In addition, the full-length extracellular signal-regulated kinases (ERK) gene, which plays an important role in the MAPK pathway, was cloned in D. pulex, and the amino acid sequence, function domain, and phylogenetic tree were analyzed. The results show that nanoplastic caused the overproduction of ROS along with other dose-dependent effects. Low nanoplastic concentrations (0.1 and/or 0.5 mg/L) significantly increased the expressions of genes of the MAPK pathway (ERK; p38 mitogen-activated protein kinases, p38; c-Jun amino-terminal kinases, JNK; and protein kinase B, AKT), HIF-1 pathway ( prolyl hydroxylasedomain, PHD; vascular endothelial growth factor, VEGF; glucose transporter, GLUT; pyruvate kinase M, PKM; hypoxia-inducible factor 1, HIF1), and CuZn superoxide dismutase (SOD) along with the activity of glutathione-S-transferase. As the nanoplastic concentration increased, these indicators were significantly suppressed. The protein expression ratio of ERK, JNK, AKT, HIF1α, and NFkBp65 (nuclear transcription factor-kB p65) as well as the phosphorylation of ERK and NFkBp65 were increased in a dose-dependent manner. The activities of other antioxidant enzymes (catalase, total SOD, and CuZn SOD) were significantly decreased upon exposure to nanoplastic. Combined with our previous work, these results suggest that polystyrene nanoplastic causes the overproduction of ROS and activates the downstream pathway, resulting in inhibited growth, development, and reproduction. The present study fosters a better understanding of the biological effects of nanoplastics on zooplankton.
The growing application of gene expression profiling demands powerful yet user-friendly bioinformatics tools to support systems-level data understanding. NetworkAnalyst was first released in 2014 to address the key need for interpreting gene expression data within the context of protein-protein interaction (PPI) networks. It was soon updated for gene expression meta-analysis with improved workflow and performance. Over the years, NetworkAnalyst has been continuously updated based on community feedback and technology progresses. Users can now perform gene expression profiling for 17 different species. In addition to generic PPI networks, users can now create cell-type or tissue specific PPI networks, gene regulatory networks, gene co-expression networks as well as networks for toxicogenomics and pharmacogenomics studies. The resulting networks can be customized and explored in 2D, 3D as well as Virtual Reality (VR) space. For meta-analysis, users can now visually compare multiple gene lists through interactive heatmaps, enrichment networks, Venn diagrams or chord diagrams. In addition, users have the option to create their own data analysis projects, which can be saved and resumed at a later time. These new features are released together as NetworkAnalyst 3.0, freely available at https://www.networkanalyst.ca.
A critical component in the interpretation of systems-level studies is the inference of enriched biological pathways and protein complexes contained within OMICs datasets. Successful analysis requires the integration of a broad set of current biological databases and the application of a robust analytical pipeline to produce readily interpretable results. Metascape is a web-based portal designed to provide a comprehensive gene list annotation and analysis resource for experimental biologists. In terms of design features, Metascape combines functional enrichment, interactome analysis, gene annotation, and membership search to leverage over 40 independent knowledgebases within one integrated portal. Additionally, it facilitates comparative analyses of datasets across multiple independent and orthogonal experiments. Metascape provides a significantly simplified user experience through a one-click Express Analysis interface to generate interpretable outputs. Taken together, Metascape is an effective and efficient tool for experimental biologists to comprehensively analyze and interpret OMICs-based studies in the big data era.
Neonatal encephalopathy due to hypoxia ischemia (HI) leads to severe, life-long morbidities in thousands of neonates born in the US and worldwide each year. Varying capacities of long-term episodic memory, verbal working memory and learning can present without cerebral palsy and have been associated with the severity of neonatal encephalopathy sustained at birth. Among children who sustain a moderate degree of HI at birth, girls have larger hippocampal volumes compared to boys. Clinical studies indicate that female neonatal brains are more resistant to the effects of neonatal HI, resulting in better long-term cognitive outcomes as compared to males with comparable brain injury. Our most recent mechanistic studies have addressed the origins and cellular basis of sex differences in hippocampal neuroprotection following neonatal HI-related brain injury, and implicate estrogen receptor α(ERα) in the neurotrophin receptor-mediated hippocampal neuroprotection in female mice. This review summarizes the recent findings on ERα dependent, neurotrophin-mediated hippocampal neuroprotection, and weighs the evidence that this mechanism plays an important role in preserving long-term memory and learning following HI in females.
Emerging evidence now indicates that mitochondria are central regulators of neural stem cell (NSC) fate decisions and are crucial for both neurodevelopment and adult neurogenesis, which in turn contribute to cognitive processes in the mature brain. Inherited mutations and accumulated damage to mitochondria over the course of ageing serve as key factors underlying cognitive defects in neurodevelopmental disorders and neurodegenerative diseases, respectively. In this Review, we explore the recent findings that implicate mitochondria as crucial regulators of NSC function and cognition. In this respect, mitochondria may serve as targets for stem-cell-based therapies and interventions for cognitive defects.
Little is known about how 17β-estradiol (E2) mediates memory formation in males. In ovariectomized (OVX) mice, bilateral dorsal hippocampal (DH) infusion of E2 enhances memory consolidation in object recognition (OR) and object placement (OP) tasks in a manner dependent on activation of extracellular signal-regulated kinase (ERK) and Akt signaling. Here, bilateral DH E2 infusion enhanced memory consolidation in both tasks among OVX female, gonadally-intact male, and castrated male mice, suggesting comparable facilitation of memory consolidation in both sexes, independent of testicular hormones in males. Contrary to previous reports in OVX mice, E2 did not increase DH ERK or Akt phosphorylation in males, nor did the ERK inhibitor U0126 [1,4-diamino-2,3-dicyano-1,4-bis (o-aminophenylmercapto) butadiene] prevent E2 from enhancing memory consolidation among intact and castrated males. These data suggest that ERK activation is not necessary for E2 to enhance memory consolidation in males, and compared with previous reports in females, reveal novel sex differences in the cell-signaling pathways through which E2 facilitates memory consolidation. To explore the mechanisms underlying E2-induced memory enhancements in males, phosphorylation of the transcription factor cAMP response element binding protein (CREB) in the DH was assessed. E2 increased phospho-CREB levels in both sexes, yet U0126 did not block these increases in castrated or intact males, indicating that E2 regulates CREB phosphorylation in males via an ERK-independent mechanism. Collectively, these findings suggest that the beneficial effects of hippocampal E2 on memory consolidation in males and females are mediated by different molecular mechanisms, which has important implications for the development of treatments to reduce memory dysfunction in men and women.
Piperlongumine (PL), a biologically active compound from the Piper species, has been shown to exert various pharmacological effects in a number of conditions, including tumours, diabetes, pain, psychiatric disorders and neurodegenerative disease. In this study, we evaluated the therapeutic effects of PL on hippocampal function and cognition decline in aged mice. PL (50 mg/kg/day) was intragastrically administrated to 23‑month‑old female C57BL/6J mice for 8 weeks. Novel object recognition and nest building behaviour tests were used to assess cognitive and social functions. Additionally, immunohistochemistry and western blot analysis were performed to examine the effects of PL on the hippocampus. We found that the oral administration of PL significantly improved novel object recognition and nest building behaviour in aged mice. Although neither the percentage area occupied by astrocytes and microglia nor the level of 4‑hydroxynonenal protein, a specific marker of lipid peroxidation, were altered by PL treatment, the phosphorylation levels of N‑methyl‑D‑aspartate receptor subtype 2B (NR2B), calmodulin‑dependent protein kinase II alpha (CaMKIIα) and extracellular signal‑regulated kinase 1/2 (ERK1/2) were markedly increased in the hippocampus of aged mice following the administration of PL. We also found that PL treatment resulted in a CA3‑specific increase in the phosphorylation level of cyclic AMP response element binding protein, which is recognized as a potent marker of neuronal plasticity, learning and memory. Moreover, the number of doublecortin‑positive cells, a specific marker of neurogenesis, was significantly increased following PL treatment in the dentate gyrus of the hippocampus. On the whole, these data demonstrate that PL treatment may be a potential novel approach in the treatment of age‑related cognitive impairment and hippocampal changes.
Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease (PD). LRRK2 contains a functional kinase domain and G2019S, the most prevalent LRRK2 pathogenic mutation, increases its kinase activity. LRRK2 regulates mitochondria morphology and autophagy in neurons. LPS treatment increases LRRK2 protein level and mitochondrial fission in microglia, and down-regulation of LRRK2 expression or inhibition of its kinase activity attenuates microglia activation. Here, we evaluated the direct role of LRRK2 G2019S in mitochondrial dynamics in microglia. Initial observation of microglia in G2019S transgenic mice revealed a decrease in mitochondrial area and shortage of microglial processes compared with their littermates. Next, we elucidated the molecular mechanisms of these phenotypes. Treatment of BV2 cells and primary microglia with LPS enhanced mitochondrial fission and increased Drp1, a mitochondrial fission marker, as previously reported. Importantly, both phenotypes were rescued by treatment with GSK2578215A, a LRRK2 kinase inhibitor. Finally, the protein levels of CD68, an active microglia marker, Drp1 and TNF-α were significantly higher in brain lysates of G2019S transgenic mice compared with the levels in their littermates. Taken together, our data suggest that LRRK2 could promote microglial mitochondrial alteration via Drp1 in a kinase-dependent manner, resulting in stimulation of pro-inflammatory responses. This mechanism in microglia might be a potential target to develop PD therapy since neuroinflammation by active microglia is a major symptom of PD.
Properties of the local internal environment of the adult brain are tightly controlled providing a stable milieu essential for its normal function. The mechanisms involved in this complex control are structural, molecular and physiological (influx and efflux transporters) frequently referred to as the “blood‐brain barrier”. These mechanisms include regulation of ion levels in brain interstitial fluid essential for normal neuronal function, supply of nutrients, removal of metabolic products and prevention of entry or elimination of toxic agents. A key feature is cerebrospinal fluid secretion and turnover. This is much less during development, allowing greater accumulation of permeating molecules. The overall effect of these mechanisms is to tightly control the exchange of molecules into and out of the brain. This review presents experimental evidence currently available on the status of these mechanisms in developing brain. It has been frequently stated for over nearly a century that the blood‐brain barrier is not present or at least is functionally deficient in the embryo, fetus and newborn. We suggest the alternative hypothesis that the barrier mechanisms in developing brain are likely to be appropriately matched to each stage of its development. The contributions of different barrier mechanisms, such as changes in constituents of cerebrospinal fluid in relation to specific features of brain development, for example neurogenesis, are only beginning to be studied. The evidence on this previously neglected aspect of brain barrier function is outlined. We also suggest future directions this field could follow with special emphasis on potential applications in a clinical setting. This article is protected by copyright. All rights reserved
Recently, we have reported that animals with telomerase reverse transcriptase (TERT) overexpression exhibit reduced social interaction, decreased preference for novel social interaction and poor nest-building behaviors-symptoms that mirror those observed in human autism spectrum disorders (ASD). Overexpression of TERT also alters the excitatory/inhibitory (E/I) ratio in the medial prefrontal cortex. However, the effects of TERT overexpression on hippocampal-dependent learning and synaptic efficacy have not been investigated. In the present study, we employed electrophysiological approaches in combination with behavioral analysis to examine hippocampal function of TERT transgenic (TERT-tg) mice and FVB controls. We found that TERT overexpression results in enhanced hippocampal excitation with no changes in inhibition and significantly impairs long-term synaptic plasticity. Interestingly, the expression levels of phosphorylated CREB and phosphorylated CaMKIIα were significantly decreased while the expression level of CaMKIIα was slightly increased in the hippocampus of TERT-overexpressing mice. Our observations highlight the importance of TERT in normal synaptic function and behavior and provide additional information on a novel animal model of ASD associated with TERT overexpression.
Polymer-based multilayer packaging materials are commonly used in order to combine the respective performance of different polymers. By this approach, the tailored functionality of packaging concepts is created to sufficiently protect sensitive food products and thus obtain extended shelf life. However, because of their poor recyclability, most multilayers are usually incinerated or landfilled, counteracting the efforts towards a circular economy and crude oil independency. This review depicts the current state of the European multilayer packaging market and sketches the current end-of-life situation of postconsumer multilayer packaging waste in Germany. In the main section, a general overview of the state of research about material recycling of different multilayer packaging systems is provided. It is divided into two subsections, whereby one describes methods to achieve a separation of the different components, either by delamination or the selective dissolution–reprecipitation technique, and the other describes methods to achieve recycling by compatibilization of nonmiscible polymer types. While compatibilization methods and the technique of dissolution–reprecipitation are already extensively studied, the delamination of packaging has not been investigated systematically. All the presented options are able to recycle multilayer packaging, but also have drawbacks like a limited scope or a high expenditure of energy.
Abnormal potentiation in the lateral habenula (LHb) has been suggested to mediate depression-like behaviors. However, the underlying mechanisms of the synaptic efficacy regulation of LHb synapses and the potential for their modulation are only poorly understood. Here, we report that long-term synaptic depression (LTD) occurs in the LHb upon both low-frequency stimulation (LFS) and moderate-frequency stimulation (MFS). LFS-induced LTD (LFS-LTD) is accompanied by a reduction in presynaptic release probability, which is endocannabinoid (eCB) signaling dependent. Surprisingly, exposure to an acute stressor completely masks the induction of LFS-LTD in the LHb while leaving the MFS-induced LTD intact. Pharmacological activation of cannabinoid receptor 1 (CB1R) or blockade of αCaMKII successfully restored LTD in the LHb in an animal model of depression. Thus, our findings reveal a form of synaptic strength regulation and a stress-induced shift of synaptic plasticity in the LHb.
Mitochondrial dysfunction is a common feature of many genetic disorders that target the brain and cognition. However, the exact role these organelles play in the etiology of such disorders is not understood. Here we show that mitochondrial dysfunction impairs brain development, depletes the adult neural stem cell (NSC) pool and impacts embryonic and adult neurogenesis. Using deletion of the mitochondrial oxidoreductase AIF as a genetic model of mitochondrial and neurodegenerative diseases revealed the importance of mitochondria in multiple steps of the neurogenic process. Developmentally, impaired mitochondrial function causes defects in NSC self-renewal, neural progenitor cell (NPC) proliferation and cell cycle exit, as well as neuronal differentiation. Sustained mitochondrial dysfunction into adulthood leads to NSC depletion, loss of adult neurogenesis and manifests as a decline in brain function and cognitive impairment. These data demonstrate that mitochondrial dysfunction, as observed in genetic mitochondrial and neurodegenerative diseases, underlies the decline of brain function and cognition due to impaired stem cell maintenance and neurogenesis.
Microplastics (MPs) are a significant environmental health issue and increasingly greater source of concern. MPs have been detected in oceans, rivers, sediments, sewages, soil and even table salts. MPs exposure on marine organisms and humans has been documented, but information about the toxicity of MPs in mammal is limited. Here we used fluorescent and pristine polystyrene microplastics (PS-MPs) particles with two diameters (5 μm and 20 μm) to investigate the tissue distribution, accumulation, and tissue-specific health risk of MPs in mice. Results indicated that MPs accumulated in liver, kidney and gut, with a tissue-accumulation kinetics and distribution pattern that was strongly depended on the MPs particle size. In addition, analyses of multiple biochemical biomarkers and metabolomic profiles suggested that MPs exposure induced disturbance of energy and lipid metabolism as well as oxidative stress. Interestingly, blood biomarkers of neurotoxicity were also altered. Our results uncovered the distribution and accumulation of MPs across mice tissues and revealed significant alteration in several biomarkers that indicate potential toxicity from MPs exposure. Collectively, our data provided new evidence for the adverse consequences of MPs.
Humulus japonicus Siebold & Zucc. (HJ) has traditionally been administered to patients with pulmonary disease, skin disease and hypertension in Korea, and it is considered to exert anti-inflammatory, antioxidant, antimicrobial and anti-mycobacterial effects. However, its effects against Alzheimer's disease (AD) have yet to be explored. Thus, this study was carried out to investigate whether HJ has a beneficial effect on the progression of AD in an animal model. A methanolic extract of HJ (500 mg/kg/day) was intragastrically administered to 5-month-old APP/PS1 transgenic (Tg-APP/PS1) mice for 2.5 months. Novel object recognition and Y-maze alteration tests were used to assess cognitive function, and an immunohistochemical assay was performed to assess amyloid β (Aβ) deposition, tau phosphorylation and gliosis. An in vitro assay using a microglial cell line was also performed to investigate the anti-inflammatory effects of HJ. Our results revealed that HJ significantly decreased the mRNA and protein expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and inducible nitric oxide synthase (iNOS) induced by lipopolysaccharide in the microglial cell line. The administration of HJ for 2 months improved the cognitive function of Tg-APP/PS1 mice. HJ notably reduced the area occupied by Aβ and neurofibrillary tangles, and the number of activated astrocytes and microglia in the cortex of Tg-APP/PS1 mice. The findings of our study suggest that HJ has the therapeutic potential to inhibit the progression of AD and to improve cognitive deterioration in Tg-APP/PS1 mice.
Children in America today are at an unacceptably high risk of developing neurodevelopmental disorders that affect the brain and nervous system including autism, attention deficit hyperactivity disorder, intellectual disabilities, and other learning and behavioral disabilities. These are complex disorders with multiple causes—genetic, social, and environmental. The contribution of toxic chemicals to these disorders can be prevented. Approach: Leading scientific and medical experts, along with children’s health advocates, came together in 2015 under the auspices of Project TENDR: Targeting Environmental Neuro-Developmental Risks to issue a call to action to reduce widespread exposures to chemicals that interfere with fetal and children’s brain development. Based on the available scientific evidence, the TENDR authors have identified prime examples of toxic chemicals and pollutants that increase children’s risks for neurodevelopmental disorders. These include chemicals that are used extensively in consumer products and that have become widespread in the environment. Some are chemicals to which children and pregnant women are regularly exposed, and they are detected in the bodies of virtually all Americans in national surveys conducted by the U.S. Centers for Disease Control and Prevention. The vast majority of chemicals in industrial and consumer products undergo almost no testing for developmental neurotoxicity or other health effects. Conclusion: Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. These measures are urgently needed if we are to protect healthy brain development so that current and future generations can reach their fullest potential.
Rapid modulation of hippocampal synaptic plasticity through synaptic estrogen receptors is an essential topic. We analyzed estradiol-induced modulation of CA1 dendritic spines using adult male ERαKO and ERβKO mice. A 2h treatment of estradiol particularly increased the density of middle-head spines (diameter 0.3-0.4µm) in wild type mouse hippocampal slices. The enhancement of spinogenesis was completely suppressed by MAP kinase inhibitor. Estradiol-induced increase in middle-head spines was observed in ERβKO mice (which express ERα), but not in ERαKO, indicating that ERα is necessary for the spinogenesis. Direct observation of the dynamic estradiol-induced enhancing effect on rapid spinogenesis was performed using time-lapse imaging of spines in hippocampal live slices from yellow fluorescent protein expressed mice. Both appearance and disappearance of spines occurred, and the number of newly appeared spines was significantly greater than that of disappeared spines, resulting in the net increase of the spine density within 2h. As another type of synaptic modulation, we observed that estradiol rapidly enhanced N-methyl-D-aspartate (NMDA)-induced long-term depression (LTD) in CA1 of the wild type mouse hippocampus. In contrast, estradiol did not enhance NMDA-LTD in ERαKO mice, indicating the involvement of ERα in the estrogen signaling. This article is part of a Special Issue entitled SI: Brain and Memory.
Copyright © 2014. Published by Elsevier B.V.
TopHat is a popular spliced aligner for RNA-seq experiments. Here, we describe TopHat2, which incorporates many significant enhancements to TopHat. TopHat2 can align reads of various lengths produced by the latest sequencing technologies, while allowing for variable-length indels with respect to the reference genome. In addition to de novo spliced alignment, TopHat2 can align reads across fusion breaks, which occur after genomic translocations. TopHat2 combines the ability to discover novel splice sites with direct mapping to known transcripts, producing sensitive and accurate alignments, even for highly repetitive genomes or in the presence of pseudogenes. TopHat2 is available at http://ccb.jhu.edu/software/tophat.
The toxic mechanisms of functionalized polystyrene nanoplastics (NPs) in bivalves, especially regarding energy homeostasis and immunity in benthic marine ecosystem, are poorly understood. Therefore, in this study, the toxicity effects of two amino-modified and carboxylated polystyrene NPs (PS-NH2and PS-COOH) on clams (Meretrix meretrix) at individual, organic, cellular, and gene levels were investigated at environmentally relevant NP concentrations of 0.02-2 mg L⁻¹. The exposure of both NPs showed non-lethal effect but inhibited the clam growth. Little difference in the toxic effect was observed between the two NPs, mainly due to their similar bioaccessibility. The inhibition of clam growth was mainly driven by the energy homeostasis imbalanceviathe atrophic inflammation of digestive glands induced by the bioaccumulation of NPs. The immunomodulation dysfunction, manifested as decreased phagocytosis resulting from the lysosomal membrane destabilization, was also responsible for the inhibited growth. Furthermore, the mechanisms of genotoxicity were identified to be energy homeostasis imbalance triggered by pancreatic secretion, tricarboxylic acid cycle (TCA) cycle, and peroxisome proliferator activated-receptor α (PPARα) signaling pathway, and the immunomodulation dysregulation dominated by the constrained toll-like receptors (TLR) and nuclear factor-kappa B (NF-κB) signaling pathway, phagosome and lysosome pathway. This work has expanded the current understanding of the toxic mechanisms of functionalized NPs in bivalves, highlighting the potential risks of the NPs in the stability and function of marine benthic ecosystems, even food security.
Microplastics which are gradually and randomly decompose into small fragment by exposure of physical and biological external stress are emerging as a significant threat to the all the environments. Here, we have demonstrated the in vitro toxicity of microplastics of two different shapes. To minimize the chemical effect, polyethylene (PE), was used. PE microplastics with two different shapes were prepared, high-density PE microbeads and irregularly ground low-density PE from bulk pellets. It is hypothesized that morphological characteristics and concentration of PE microplastics could affect cellular viability, immunity, and lysis. To quantify the randomness of the microplastic shape, the edge patterns of the generated PE microplastics were converted into numerical values and analyzed using a statistical method. A 10-fold difference in curvature value was observed between microbeads and ground microfragments. To correlate shape differences to toxicology, cells were exposed to PE microplastics on the demand of toxicology studies. We found that the higher concentration and rough structure were associated with the toxicity of plastics toward cells, pro-inflammatory cytokine release, and hemolysis, even though PE is buoyant onto medium. The PE microbeads did not exhibit severe cytotoxicity at any of the tested concentrations, but induced immune and hemolysis responses at high concentrations. When comparing the toxicity of different shapes of PE microplastics, we confirmed by statistical analysis that irregular-shape plastics with sharp edges and higher curvature differences may adversely affect cells, further having possibility to human toxicity in real environment.
Background:
Women are reported more likely to develop depression and dementia. However, the involved mechanism is poorly understood.
Objective:
Here, we clarified the role of estrogen receptor α (ERα) in depression and cognitive deficit in young female rats.
Methods:
After being exposed to 7-weeks' chronic unpredicted mild stress (CUMS), the depression resilient rats (Res rats) and depressed rats (Dep rats) were selected according to their records in sucrose preference test, forced swimming test, and open field test. Their cognition abilities were tested by Morris water maze. Proteomic assay, immunoprecipitation, western blotting, immunohistochemical, and Nissl staining were also used to understand the involved mechanism.
Results:
Compared with control rats and Res rats, Dep rats showed cognitive deficits and hippocampal impairments revealed by proteomic data, neuron losses, increased cleaved caspase-3, β-catenin phosphorylation, and glycogen synthase kinase3β (GSK3β) activation. As ERα, but not ERb, was found declined in hippocampi of Dep rats, 4,4k,4a-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT, an ERα agonist, 1 mg/kg/day), was used to treat Dep rats (Dep + PPT). Twenty days later, the depressive behaviors, cognition deficits, and hippocampal neuron loss were rescued in Dep + PPT rats. Furthermore, Res and Dep + PPT rats had higher levels of β-catenin combined with ERα and lower levels of β-catenin combined with GSK3β than Dep rats in hippocampi.
Conclusion:
These results demonstrated hippocampal ERα is an important pro-resilient factor in CUMS-induced depressive behaviors and cognitive deficits. It was also given that the neuroprotection afforded by hippocampal ERα/Wnt interactions have significant implications for cognition and emotion in young females.
Microplastics (MPs) have become hazardous materials, which have aroused widespread concern about their potential toxicity. However, the effects of MPs on reproductive systems in mammals are still ambiguous. In this study, the toxic effects of polystyrene MPs (PS-MPs) in male reproduction of mice were investigated. The results indicated that after exposure for 24 h, 4 μm and 10 μm PS-MPs accumulated in the testis of mice. Meanwhile, 0.5 μm, 4 μm, and 10 μm PS-MPs could enter into three kinds of testicular cells in vitro. In addition, sperm quality and testosterone level of mice were declined after exposure to 0.5 μm, 4 μm, and 10 μm PS-MPs for 28 days. H&E staining showed that spermatogenic cells abscissed and arranged disorderly, and multinucleated gonocytes occurred in the seminiferous tubule. Moreover, PS-MPs induced testicular inflammation and the disruption of blood-testis barrier. In summary, this study demonstrated that PS-MPs induced male reproductive dysfunctions in mice, which provided new insights into the toxicity of MPs in mammals.
With the increase in plastic production, a variety of toxicological studies on microplastics have been conducted as microplastics can be accumulated in the human body and cause unknown disease. However, previous studies have mainly assessed the toxicity of sphere-type microbeads, which may differ from randomly-shaped microplastics in a real environment. Here, we conducted in vitro toxicology analysis for randomly-shaped microplastics based on the hypotheses that (1) physical cytotoxicity is affected by nano-/micro-size roughness in polystyrene (PS) microfragments and (2) chemical toxicity is caused by chemical reagents from microplastics. We confirmed that the PS microfragments increased the acute inflammation of immune cells 20 times than control, the production of reactive oxygen species, and cell death of fibroblasts and cancer cells by releasing chemical reagents. In addition, when the PS microfragments were in direct contact with fibroblasts and red blood cells, the physical stress caused by them resulted in lactose dehydrogenase and hemoglobin release, respectively, due to cell membrane damage and hemolysis. This phenomenon was amplified when the concentration and roughness of the microfragments increased. Moreover, we quantitatively analyzed roughness differences between microplastics, which revealed a strong relationship between the physical damage of cells and the roughness of microplastics.
In this study, the hypothesis that polyethylene microplastics (MPs) can accumulate in animals, reach the upper trophic level and trigger behavioral changes was tested. Physalaemus cuvieri tadpoles were exposed to MPs (for 7 days) and fed on tambatinga fish for the same period. Subsequently, these fish were given as food to Swiss mice. The MP amount in animals’ liver was quantified and results have evidenced its accumulation at all assessed trophic levels [tadpole: 18,201.9 particles/g; fish: 1.26 particles/g; mice receiving tambatingas who had fed on tadpoles exposed to MPs: 57.07 particles/g and mice receiving water added with MPs: 89.12 particles/g). Such accumulation in the last group was associated with shorter traveled distance, slower locomotion speed and higher anxiety index in the open field test. Mice receiving tambatingas who had fed on tadpoles exposed to MPs were confronted to a potential predator and showed responses similar to those of animals who had ingested water added with MPs (lack of defensive social aggregation and reduced risk assessment behavior). Thus, results have preliminarily confirmed the initial hypothesis about how MPs in water can reach terrestrial trophic levels and have negative impact on the survival of these animals.
Microplastics as new emerging pollutants in aquatic environments have received much attention in recent years. However, up to now, microplastic contamination in tap water has only been investigated by few studies. Therefore, this study investigated the presence of microplastics in tap water. 38 tap water samples were taken at different cities of China. The amount of microplastics in tap water varied from 440 ± 275 particles L⁻¹. Particles smaller than 50 μm significantly predominated in most of the tap water samples. Further, according to the shape of these particles, fragments, fibers and spheres were found in tap water samples, while fragments were the most abundant morphotype in most samples. Despite these particles were identified as 14 different materials by micro-Raman spectroscopy, the majority of the microplastics comprised of polyethylene and polypropylene. Based on this investigation, drinking water treatment plants seemingly have to face the problem of microplastic pollution in tap water due to their potential eco-toxicological effects on humans.
Microplastics are ubiquitous across ecosystems, yet the exposure risk to humans is unresolved. Focusing on the American diet, we evaluated the number of microplastic particles in commonly consumed foods in relation to their recommended daily intake. The potential for microplastic inhalation and how the source of drinking water may affect microplastic consumption were also explored. Our analysis used 402 data points from 26 studies, which represents over 3600 processed samples. Evaluating approximately 15% of Americans' caloric intake, we estimate that annual microplastics consumption ranges from 39000 to 52000 particles depending on age and sex. These estimates increase to 74000 and 121000 when inhalation is considered. Additionally, individuals who meet their recommended water intake through only bottled sources may be ingesting an additional 90000 microplastics annually, compared to 4000 microplastics for those who consume only tap water. These estimates are subject to large amounts of variation; however, given methodological and data limitations, these values are likely underestimates.
Spastin is a microtubule-severing enzyme encoded by SPAST, which is broadly expressed in various cell types originated from multiple organs. Even though SPAST is well known as a regulator of the axon growth and arborization in neurons and a genetic factor of hereditary spastic paraplegia, it also takes part in a wide range of other cellular functions including the regulation of cell division and proliferation. In this study, we investigated a novel biological role of spastin in developing brain using Spast deficient mouse embryonic neural stem cells (NSCs) and perinatal mouse brain. We found that the expression of spastin begins at early embryonic stages in mouse brain. Using Spast shRNA treated NSCs and mouse brain, we sh