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Fenton and Haber-Weiss reactions are a source of oxidative stress. The generation of oxygen free radicals occurs first with the reduction of ferric to ferrous iron and then by the Fenton reaction with ferrous iron catalyzing the breakdown of hydrogen peroxide to hydroxyl radical and hydroxyl. The net reaction is termed the Haber-Weiss reaction.
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Iron homeostasis is often disrupted in acute disease with an increase in catalytic free iron leading to the formation of reactive oxygen species and subsequent tissue-specific oxidative damage. This article highlights the potential therapeutic benefit of exogenous hepcidin to prevent and treat iron-induced injury, specifically in the management of...
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... iron (CFI) is undetectable and plasma iron is tightly bound to TF. CFI, which can be thought of as unbound iron, is a promiscuous molecule that functions as a "bad-actor." When CFI is in its ferrous state (Fe 21 ), CFI can initiate the Fenton reactions or when iron is unbound in its ferric state (Fe 31 ) CFI can initiate Haber-Weiss reactions (Fig. 2). These reactions generate oxygen free radicals, such as hydroxyl radical (OH À ), peroxynitrite (ONOO À ), superoxide free radical anion (O 2 À ), and hydrogen peroxide (H 2 O 2 ). 23,24 These oxygen free radicals are often referred to as reactive oxygen species (ROS) and can damage important macromolecules. ROS have been shown to ...
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... [106] Conversely, the delivery of hepcidin is viewed as a prospective treatment approach for preventing and managing AKI within intensive care units. [107] In addition, an increasing amount of data suggests that ferroptosis is involved in AKI. [108] Under normal physiological conditions, redox reactions in lipids and oxylipids serve as highly diverse signals for various processes. ...
Acute kidney injury (AKI) represents a substantial challenge to public health and is characterized by elevated occurrence and fatality rates. In the last 3 decades, the disruption of iron homeostasis and the cytotoxic effects mediated by iron have been extensively acknowledged as contributors to, as well as outcomes of, renal damage. Therefore, iron metabolism has become the focus of novel therapeutic interventions for AKI, with targeted iron metabolism strategies showing great potential. In this review, we have explored the dysregulation of iron metabolism in AKI and the AKI caused by iron metabolism disorders. We have summarized the complex mechanisms of iron metabolism in the kidney and emphasized the potential role of iron metabolism‐related metabolic pathways in the treatment and prevention of AKI. Finally, we have reviewed various strategies targeting iron metabolism for the treatment of AKI, hoping to provide more effective treatment options for AKI patients in the future.
... The oxidative stress in the vascular endothelium is mediated by superoxide anions (O 2 •− ) [45], hydroxyl species (HO − ), and hydrogen peroxide (H 2 O 2 ) [46]. The O 2 •− may react with NO •− , forming peroxynitrite radicals (ONOO − ) [47], which leads to endothelial nitric oxide synthase (eNOS) uncoupling and further O 2 ...
... The O 2 •− can also participate in the Haber-Weiss reaction, which interacts with H 2 O 2 to produce HO. [46]. Superoxide dismutase (SOD) is critical for the O 2 ...
... Xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) also produced HO − . The HO − is cleared by catalase (CAT), glutathione peroxidase (GPX), and the thioredoxin (TRX) system [46,48,49]. The sources of ROS production are the mitochondrial activity at complexes 1 and 3, NOX, XO [50], and uncoupled eNOS [51,52], as well as the Fenton and Haber-Weiss reactions, which generate hydroxyl radicals and contribute to oxidative damage [53]. ...
The "One Health approach" has evidenced the significant impact of xenobiotic exposure to health, and humans are a relevant target for their toxic effects. Bisphenol A (BPA) exerts a ubiquitous exposure source in all ecosystems. Given its endocrine-disrupting and harmful consequences on health, several countries have enforced new regulations to reduce exposure to BPA. Cardiovascular diseases (CVDs) are complex conditions that lead to higher mortality worldwide, where family history, lifestyle, and environmental factors, like BPA exposure, have a remarkable contribution. This chemical compound is the most widely used in plastic and epoxy resin manufacturing and has been associated with effects on human health. Therefore, new-generation bisphenols (NGBs) are replacing BPA use, arguing that they do not harm health. Nonetheless, the knowledge about whether NGBs are secure options is scanty. Although BPA's effects on several organs and systems have been documented, the role of BPA and NGBs in CVDs has yet to be explored. This review's goals are focused on the processes of endothelial activation (EA)-endothelial dysfunction (ED), a cornerstone of CVDs development, bisphenols' (BPs) effects on these processes through oxidant and antioxidant system alteration, and the potential benefits of antioxidant compounds to mitigate BPs' effects on the CVS. Despite the scarce evidence on pro-oxidant effects associated with NGBs, our review demonstrated a comparable harmful effect on BPA. The results from the present review suggest that the biological mechanisms proposed by BPs to explain their cardiotoxic effects are the oxidant stress ↔ inflammatory response ↔ EA ↔ ED → atherosclerotic plate → coagulation promotion. Other effects contributing to CVD development include altered lipid metabolism, ionic channels, and the activation of different intracellular pathways, which contribute to ED perpetuation in a concerted manner.
... Immunocompetent cells see MNPs as a hazard and respond by generating ROS as a defense mechanism. As signal transducers, MNPs can stimulate cellular pathways involved in ROS generation, just as transition metals can trigger ROS generation by participating in Fenton and Haber-Weiss processes (Chawla et al., 2019;Canaparo et al., 2021). Electron leakage occurs when MNPs interrupt the mitochondrial electron transport chain, which allows free electrons to create ROS from oxygen particles (Gallud et al., 2019). ...
Metallic nanoparticles (MNPs) have garnered significant attention due to their ability to improve the therapeutic index of medications by reducing multidrug resistance and effectively delivering therapeutic agents through active targeting. In addition to drug delivery, MNPs have several medical applications, including in vitro and in vivo diagnostics, and they improve the biocompatibility of materials and nutraceuticals. MNPs have several advantages in drug delivery systems and genetic manipulation, such as improved stability and half-life in circulation, passive or active targeting into the desired target selective tissue, and gene manipulation by delivering genetic materials. The main goal of this review is to provide current information on the present issues and prospects of MNPs in drug and gene delivery systems. The current study focused on MNP preparation methods and their characterization by different techniques, their applications to targeted delivery, non-viral vectors in genetic manipulation, and challenges in clinical trial translation.
... One proposed mechanism of CuNPinduced microbial death is the induction of reactive oxygen species (ROS) through Fenton-like and Haber-Weiss reactions. [54,55] These are singlet oxygen ( 1 O 2 ), hydroxyl radicals (•OH), hydrogen peroxide (H 2 O 2 ), and superoxide radicals ( • O 2 ) that are derived from molecular oxygen and can be quenched through endogenous systems. In this scenario, the number of ROS formed outweighs the cell's capacity to remove them, leading to oxidative stress that can cause irreversible damage to the bacteria resulting in cell death. ...
The prevalence of the SARS‐CoV‐2 virus has led to an increased focus on cleaning and disinfecting surfaces in the community and hospitals. An inherently antibacterial thin film is reported to combat the transmission of microbes on glass surfaces that could be accessed by the public, reducing the need for constant cleaning. The copper nanoparticle thin film is synthesized via a sol–gel method and deposited using a dip‐coater to create a transparent, rugged film resistant to scratching. The antibacterial performance is tested by a droplet and an aerosol deposition technique, where Escherichia coli and Staphylococcus aureus are sprayed directly onto the thin film, replicating coughs and sneezes: a common form of microbial transmission. The mechanism of antibacterial performance is studied by introducing reactive oxygen species quenchers to the thin film. This research presents copper nanoparticle thin films as an effective solution in reducing the transmission of microbes on glass surfaces and their potential as a valuable tool in preventing the spread of infectious diseases.
... Further investigation is required to determine its protective role against human AKI due to the limited and conflicting available data [87]. On the other hand, the administration of hepcidin has been considered a potential therapeutic target for the prevention and treatment of AKI in the ICU [105]. The use of exogenous hepcidin could restore iron homeostasis by increasing ferritin expression and iron sequestration, leading to renal protection and a reduction in renal oxidative stress and inflammation in animal models of AKI [106,107]. ...
The multiple roles of iron in the body have been known for decades, particularly its involvement in iron overload diseases such as hemochromatosis. More recently, compelling evidence has emerged regarding the critical role of non-transferrin bound iron (NTBI), also known as catalytic iron, in the care of critically ill patients in intensive care units (ICUs). These trace amounts of iron constitute a small percentage of the serum iron, yet they are heavily implicated in the exacerbation of diseases, primarily by catalyzing the formation of reactive oxygen species, which promote oxidative stress. Additionally, catalytic iron activates macrophages and facilitates the growth of pathogens. This review aims to shed light on this underappreciated phenomenon and explore the various common sources of NTBI in ICU patients, which lead to transient iron dysregulation during acute phases of disease. Iron serves as the linchpin of a vicious cycle in many ICU pathologies that are often multifactorial. The clinical evidence showing its detrimental impact on patient outcomes will be outlined in the major ICU pathologies. Finally, different therapeutic strategies will be reviewed, including the targeting of proteins involved in iron metabolism, conventional chelation therapy, and the combination of renal replacement therapy with chelation therapy.
... Iron chelators have been previously suggested as a potential adjunct therapy in murine models, preferably together with conventional antibiotics [100][101][102][103][104]. However, their toxicity and potential to deliver iron to the bacteria limit their use [105]. To overcome these limitations, exogenous administration of hepcidin has been suggested as an alternative to the body's natural hypoferremic pathways. ...
... This therapeutic modality is expected to be less toxic and more efficient. Alternately, endogenous hepcidin induction may be achieved by catecholamines (such as norepinephrine and dopamine) administration [105]. Hepcidin can be used in conjunction with standard therapy in patients with iron overload, suffering from deadly infections of siderophilic Gram-negative bacilli, such as Yersinia enterocolitica, Vibrio vulnificus, and Klebsiella pneumoniae. ...
The emergence of antibiotic-resistant bacteria is a pressing public health concern, highlighting the need for alternative approaches to control bacterial infections. Promising approaches include the development of therapeutic vaccines and the utilization of innate immune activation techniques, which may prove useful in conjunction with antibiotics, as well as other antibacterial modalities. However, innate activation should be fast and self- or actively- contained to prevent detrimental consequences. TLR ligand adjuvants are effective at rapidly activating, within minutes to hours, the innate immune system by inducing cytokine production and other signaling molecules that bolster the host's immune response. Neutrophils serve as the first line of defense against invading pathogens by capturing and destroying them through various mechanisms, such as phagocytosis, intracellular degradation, and the formation of NETs. Nutritional immunity is another host defense mechanism that limits the availability of essential metals, such as iron, from invading bacterial pathogens. Thus, iron starvation has been proposed as a potential antibacterial strategy. In this review, we focus on approaches that have the potential to enhance rapid and precise antibacterial responses, bridging the gap between the onset of infection and the elimination of bacteria, hence limiting the infection by antibiotic-resistant bacteria.
... Iron has been thought to contribute to both AKI and CKD [113][114][115][116][117][118]. Indeed, it has been observed that renal tubules are exposed to elevated levels of iron in patients with kidney disease, which is likely due to increased filtration of iron and iron-containing proteins through the glomerular apparatus [114,117,119]. ...
The kidney is a crucial organ that eliminates metabolic waste and reabsorbs nutritious elements. It also participates in the regulation of blood pressure, maintenance of electrolyte balance and blood pH homeostasis, as well as erythropoiesis and vitamin D maturation. Due to such a heavy workload, the kidney is an energy-demanding organ and is constantly exposed to endogenous and exogenous insults, leading to the development of either acute kidney injury (AKI) or chronic kidney disease (CKD). Nevertheless, there are no therapeutic managements to treat AKI or CKD effectively. Therefore, novel therapeutic approaches for fighting kidney injury are urgently needed. This review article discusses the role of α-lipoic acid (ALA) in preventing and treating kidney diseases. We focus on various animal models of kidney injury by which the underlying renoprotective mechanisms of ALA have been unraveled. The animal models covered include diabetic nephropathy, sepsis-induced kidney injury, renal ischemic injury, unilateral ureteral obstruction, and kidney injuries induced by folic acid and metals such as cisplatin, cadmium, and iron. We highlight the common mechanisms of ALA’s renal protective actions that include decreasing oxidative damage, increasing antioxidant capacities, counteracting inflammation, mitigating renal fibrosis, and attenuating nephron cell death. It is by these mechanisms that ALA achieves its biological function of alleviating kidney injury and improving kidney function. Nevertheless, we also point out that more comprehensive, preclinical, and clinical studies will be needed to make ALA a better therapeutic agent for targeting kidney disorders.
... Copper effectiveness is attributed to the ability of copper ions to easily interconvert between Cu(I)/Cu(II) by Fenton-like (2) and Haber-Weiss (3) reactions [73] and generate ROS molecules, leading to lipid peroxidation, protein oxidation, and DNA damage [71]. Cu NPs, when exposed to aqueous environments, are susceptible to oxidation and through dissolution Cu + ions release from metallic Cu NPs [74]. ...
The development of effective and ecofriendly agrochemicals, including bactericides, fungicides, insecticides, and nematicides, to control pests and prevent plant diseases remains a key challenge. Nanotechnology has provided opportunities for the use of nanomaterials as components in the development of anti-phytopathogenic agents. Indeed, inorganic-based nanoparticles (INPs) are among the promising ones. They may play an effective role in targeting and killing microbes via diverse mechanisms, such as deposition on the microbe surface, destabilization of cell walls and membranes by released metal ions, and the induction of a toxic mechanism mediated by the production of reactive oxygen species. Considering the lack of new agrochemicals with novel mechanisms of action, it is of particular interest to determine and precisely depict which types of INPs are able to induce antimicrobial activity with no phytotoxicity effects, and which microbe species are affected. Therefore, this review aims to provide an update on the latest advances in research focusing on the study of several types of engineered INPs, that are well characterized (size, shape, composition, and surface features) and show promising reactivity against assorted species (bacteria, fungus, virus). Since effective strategies for plant protection and plant disease management are urgently needed, INPs can be an excellent alternative to chemical agrochemical agents as indicated by the present studies.
... Several stimuli could associate with hepcidin. Such as in hepcidin production and severe ID with the inflammation [15,16]. ...
The hepcidin is antimicrobial peptide has antimicrobial effects discover before more than a thousand years; it has a great role in iron metabolism and innate immunity. Hepcidin is a regulator of iron homeostasis. Its production is increased by iron excess and inflammation and decreased by hypoxia and anemia. Iron-loading anemias are diseases in which hepcidin is controlled by ineffective erythropoiesis and concurrent iron overload impacts. Hepcidin reacts with ferroportin. The ferroportin is found in spleen, duodenum, placenta, if the ferroportin decrease, it results in the reduced iron intake and macrophage release of iron, and using the iron which stores in the liver. Gene of human hepcidin is carried out by chromosome 19q13.1. It consists of (2637) nucleated base. HAMP gene was founded in the liver cells, in brain, trachea, heart, tonsils, and lung. Changing in the HAMP gene will produce a change in hepcidin function. The hepcidin is made many stimulators are included opposing effects exerted by pathological and physiological conditions. Hepcidin is essential for iron metabolism, understanding stricter and genetic base of hepcidin is crucial step to know iron behavior and reactions to many health statuses.
... Human physiologic systems have evolved to orchestrate a careful balance of iron binding and release that enables us to avoid injury while effectively delivering this essential nutrient to tissues. In acute illnesses, however, iron homeostasis is often disrupted and ferrous iron is produced, which contributes to tissue injury, as well as to a higher risk of bacterial infection (44,45). Many investigations, based in clinical and laboratory settings, have shown that iron supplementation causes more severe infections of Mycobacterium tuberculosis (46) but lower virulence of the enteric pathogen Citrobacter (47). ...
... If true, this phenomenon may provide a reference for the development of strategies to reduce S. maltophilia infection or spread. Many c-di-GMP effectors, but few in comparison to c-di-GMP turnover enzymes, have been identified, which include transcription factors, HKs, RRs, riboswitches, and degenerated DGCs and PDEs (43,44). Among the reported c-di-GMP binding HKs and RRs, distinct domains are used to interact with c-di-GMP. ...
Stenotrophomonas maltophilia has become a great threat to human health because of the high mortality of infected patients. Swimming motility plays a crucial role in regulating bacterial virulence and adaptation.