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Dose‐Dependent Hepatorenal Damage Induced by Erythrosine: A Study of Biochemical, Oxidative Stress, DNA Damage, and Histopathological Effects in Wistar Rats
Abstract
This study aimed to provide insights into the hepatorenal toxicity induced by erythrosine, a synthetic red dye commonly used in food and pharmaceuticals, which has raised concerns over its potential health risks. Twenty‐four rats were randomly divided into four groups ( n = 6). The first group was the control group and the other group received one of three doses of erythrosine based on acceptable daily intake (¼ ADI, ½ ADI, and ADI, 0.1 mg/kg body weight). This study examined biological activity via biochemical enzyme analysis, oxidative stress indices, DNA damage, and histopathology. Compared with the control group, erythrosine administration increased the serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, total protein, urea, creatinine, and uric acid at the highest erythrosine dose. The catalase and the superoxide dismutase activity decreased in both tissues at the highest dose. The glutathione‐S‐transferase activity increased at the ¼ ADI dose and decreased at higher doses in both tissues. In contrast, acetylcholinesterase activity was greater in erythrosine‐treated rats than in control rats. Oxidative stress indices indicated increased lipid peroxidation, hydrogen peroxide content, and lactate dehydrogenase activity. The comet assay was used to assess DNA damage, revealing significant damage in the erythrosine‐treated groups. Histopathological examination revealed necrotic and degenerative changes in the liver and kidney tissues. The findings underscore dose‐dependent hepatorenal toxicity and highlight the novelty of demonstrating a comprehensive link between erythrosine exposure, oxidative stress, and DNA damage. These results emphasize the need for cautious evaluation of synthetic dye consumption due to potential health risks.
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The incidence of colorectal cancer (CRC) among young people has been on the rise for the past four decades and its underlying causes are only just starting to be uncovered. Recent studies suggest that consuming ultra-processed foods and pro-inflammatory diets may be contributing factors. The increase in the use of synthetic food colors in such foods over the past 40 years, including the common synthetic food dye Allura Red AC (Red 40), coincides with the rise of early-onset colorectal cancer (EOCRC). As these ultra-processed foods are particularly appealing to children, there is a growing concern about the impact of synthetic food dyes on the development of CRC. Our study aimed to investigate the effects of Red 40 on DNA damage, the microbiome, and colonic inflammation. Despite a lack of prior research, high levels of human exposure to pro-inflammatory foods containing Red 40 highlight the urgency of exploring this issue. Our results show that Red 40 damages DNA both in vitro and in vivo and that consumption of Red 40 in the presence of a high-fat diet for 10 months leads to dysbiosis and low-grade colonic inflammation in mice. This evidence supports the hypothesis that Red 40 is a dangerous compound that dysregulates key players involved in the development of EOCRC.
Aim: To evaluate chronic exposure of carmoisine at ADI doses on some hepatocellular and renal parameters of male and female albino rats as well as to determine sex-dependent toxicity. Study Design: The study involves treatment for 30, 60, and 90 days. Each phase consists of 40 rats, divided into treatment and control groups. The treated groups were orally administered with 4.0 mg/kg of carmoisine daily for the periods of 30, 60, and 90 days. Methodology: At the end of the treatment, the rats were allowed to fast for 18 hours followed by the collection of 5 ml of whole blood specimens by means of cardiac puncture into Lithium Heparin bottles and fluoride oxalate bottles (for glucose only). Plasma obtained was analyzed for glucose (GLU), AST, ALT, ALP, creatinine (CRT), and urea. Hepatic and Renal tissues collected were fixed in 10% formol saline and later examined histologically using H&E stain. Statistical data analysis was done using GraphPad Prism version 9.02. Results: Glucose indicated significant increases after 30, 60, and 90 days of chronic treatment at ADI doses. Urea, Creatinine, AST, ALT and ALP showed significantly higher values after 60 and 90 days of treatment (except creatinine in male rats and ALP in female rats after 60 and 90 days respectively). Hepatic distortions, vacuolation, compression of central vein were seen in the liver section while distortion of proximal and distal tubules, and inflammation of the glomerulus were observed in the renal tissue of the treated rats. Conclusion: The administration of camoisine over a period of 30 days at ADI dose did not indicate hepatocellullar and renal derangements as well histological distortions in liver, and kidneys. However, after 60 and 90 days, mild hepatocellular, and renal derangements were seen. No sex-dependent toxicity was observed.
Concern that synthetic food dyes may impact behavior in children prompted a review by the California Office of Environmental Health Hazard Assessment (OEHHA). OEHHA conducted a systematic review of the epidemiologic research on synthetic food dyes and neurobehavioral outcomes in children with or without identified behavioral disorders (particularly attention and activity). We also conducted a search of the animal toxicology literature to identify studies of neurobehavioral effects in laboratory animals exposed to synthetic food dyes. Finally, we conducted a hazard characterization of the potential neurobehavioral impacts of food dye consumption. We identified 27 clinical trials of children exposed to synthetic food dyes in this review, of which 25 were challenge studies. All studies used a cross-over design and most were double blinded and the cross-over design was randomized. Sixteen (64%) out of 25 challenge studies identified some evidence of a positive association, and in 13 (52%) the association was statistically significant. These studies support a relationship between food dye exposure and adverse behavioral outcomes in children. Animal toxicology literature provides additional support for effects on behavior. Together, the human clinical trials and animal toxicology literature support an association between synthetic food dyes and behavioral impacts in children. The current Food and Drug Administration (FDA) acceptable daily intakes are based on older studies that were not designed to assess the types of behavioral effects observed in children. For four dyes where adequate dose-response data from animal and human studies were available, comparisons of the effective doses in studies that measured behavioral or brain effects following exposure to synthetic food dyes indicate that the basis of the ADIs may not be adequate to protect neurobehavior in susceptible children. There is a need to re-evaluate exposure in children and for additional research to provide a more complete database for establishing ADIs protective of neurobehavioral effects.
Simple Summary
Ecosystems have been increasingly subject to stressful conditions and thus the need to develop tools capable of assessing their impacts on populations and communities. These effects assessed at higher levels of biological organization tend to reflect the sum of effects on individuals, arising from the effects at the cellular and molecular levels. These lower biological organization levels are more responsive at an early stage, allowing them to be used as early warning endpoints to address environmental stress—biomarkers. In this work, the need to link low to high levels of biological organization is addressed and the challenges and usefulness of biomarkers in a myriad of fields discussed.
Abstract
Endpoints assessed at the population or community level are most often the result of the sum of effects on individuals, arising from the effects at the cellular and molecular levels. Within this framework, these lower biological level endpoints are more responsive at an early stage of exposure, making them potential toolboxes to be used as early-warning markers to address stress. Given this, by linking responses and understanding organisms’ metabolism and physiology, the possibilities for the use of biomarkers in stress biology are vast. Here, biomarker comprehensive examples are given to enlighten the need to link levels of biological organization, and their usefulness for a myriad of fields and applications is presented and discussed.
Erythrosine and tartrazine are one of the synthetic azo dye mostly consumed in food, drugs and other industrial compounds. This study was designed to investigate the adverse effect of combine erythrosine and tartrazine on cognitive and neurobehavioral functions, pro-oxidants, endogenous antioxidants, cholinergic system and pro-inflammatory cytokines in rats.
Erythrosine and tartrazine (2 mg/kg, 6 mg/kg, and 10 mg/kg, b.w., p.o, 50:50) was administered to rats (n = 6) for 6 weeks. Memory and neurobehavioral assessment using Novel object recognition test (NORT) and Elevated plus maze (EPM) and biochemical (pro-oxidants and anti-oxidant enzymes) and pro-inflammatory cytokine measurement from the brain sub regions namely, hippocampus and prefrontal cortex were done at the end of treatment. The results showed (p < 0.05) significant decreased memory and neurobehavioral function, increased acetyl-cholinesterase and pro-oxidants activity (Malonaldehyde level and Nitrite), decreased endogenous anti-oxidants (Glutathione and Catalase) and increased pro-inflammatory cytokines (Tumor necrosis factor-alpha, TNF-α). We suggested that the mechanism by which this oxidative and neuro-inflammatory damage and cholinergic system alteration occur might be related to the release of metabolite in fission of the azo dyes of the combined erythrosine and tartrazine administration in the animals. However, we concluded on these findings that erythrosine and tartrazine dyes significantly provoke the release of oxido-nitrergic and neuroinflammatory stress markers and also may incite acetyl-cholinesterase activities in different brain regions leading to memory and neurobehavioral impairment.
The purification of homogeneous glutathione S-transferases B and C from rat liver is described. Kinetic and physical properties of these enzymes are compared with those of homogeneous transferases A and E. The letter designations for the transferases are based on the reverse order of elution from carboxymethylcellulose, the purification step in which the transferases are separated from each other. Transferase B was purified on the basis of its ability to conjugate iodomethane with glutathione, whereas transferase C was purified on the basis of conjugation with 1,2-dichloro-4-nitrobenzene. Although each of the four enzymes can be identified by its reactivity with specific substrates, all of the enzymes are active to differing degrees in the conjugation of glutathione with p-nitrobenzyl chloride. Assay conditions for a variety of substrates are included.
All four glutathione transferases have a molecular weight of 45,000 and are dissociable into subunits of approximately 25,000 daltons. Despite the similar physical properties and overlapping substrate specificities of these enzymes, only transferases A and C are immunologically related.
The present study evaluates the regulatory effect of Nano-Curcumin (Nano-CUR) against tartrazine (TZ)-induced injuries on apoptosis-related gene expression (i.e., p⁵³, CASP-3 and CASP-9), antioxidant status, and DNA damages in bone marrow in treated rats. Male rats were arbitrarily separated into five groups, and each group was comprised of 10 rats each. The 1st group served as control (G1). The 2nd group ingested 7.5 mg TZ/kg. b.w. (body weight). The 3rd group ingested Nano-CUR 1 g/kg b.w. The 4th and 5th groups were respectively administered with (1 g Nano-CUR + 7.5 mg TZ/kg. b.w.) and (2 g Nano-CUR + 7.5 mg TZ/kg. b.w.). At the end of the experiment, blood samples, livers, and kidneys were collected. Livers and kidneys were homogenized and used for the analysis of reduced glutathione, malonaldhyde, total antioxidant capacity, lipid peroxide antioxidant enzyme activities, apoptosis-related gene expression, and genotoxicity by comit test. The ingestion of TZ for 50 days resulted in significant decreases in body, and kidney weights in rats and a relative increase in the liver weight compared to control. In contrast, the ingestion of Nano-CUR with TZ remarkably upgraded the body weight and relative liver weight compared to the normal range in the control. Aditionally, TZ ingestion in rats increased the oxidative stress biomarkers lipid peroxide (LPO) and malonaldehyde (MDA) significantly, whereas it decreased the reduced glutathione (GSH) levels and total antioxidant capacity (TAC). Similarly, the levels of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) significantly deteriorated in response to TZ ingestion. Moreover, the results revealed a remarkable up-regulation in the level of expression for the three examined genes, including p⁵³, CASP-3, and CASP-9 in TZ-ingested rats compared to the control. On the other hand, the comet assay result indicates that the ingestion of TZ induced DNA damage in bone marrow. Notably, the administration of Nano-CUR protected the kidney and liver of TZ-ingested rats as evidenced by a significant elevation in all antioxidant activities of tested enzymes (i.e, SOD, GPx, and CAT), vital recovery in GSH and TAC levels, and a statistical decrease in LPO and MDA compared to TZ-ingested rats. Interestingly, the ingestion of rats with TZ modulates the observed up-regulation in the level of expression for the chosen genes, indicating the interfering role in the signaling transduction process of TZ-mediated poisoning. The results indicate that the administration of Nano-CUR may protect against TZ-induced DNA damage in bone marrow. According to the results, Nano-CUR exerted a potential protective effect against oxidative stress, DNA damage, and the up-regulation of apoptosis-related genes induced by TZ ingested to rats.
Reproducible science requires transparent reporting. The ARRIVE guidelines (Animal Research: Reporting of In Vivo Experiments) were originally developed in 2010 to improve the reporting of animal research. They consist of a checklist of information to include in publications describing in vivo experiments to enable others to scrutinise the work adequately, evaluate its methodological rigour, and reproduce the methods and results. Despite considerable levels of endorsement by funders and journals over the years, adherence to the guidelines has been inconsistent, and the anticipated improvements in the quality of reporting in animal research publications have not been achieved. Here, we introduce ARRIVE 2.0. The guidelines have been updated and information reorganised to facilitate their use in practice. We used a Delphi exercise to prioritise and divide the items of the guidelines into 2 sets, the “ARRIVE Essential 10,” which constitutes the minimum requirement, and the “Recommended Set,” which describes the research context. This division facilitates improved reporting of animal research by supporting a stepwise approach to implementation. This helps journal editors and reviewers verify that the most important items are being reported in manuscripts. We have also developed the accompanying Explanation and Elaboration (E&E) document, which serves (1) to explain the rationale behind each item in the guidelines, (2) to clarify key concepts, and (3) to provide illustrative examples. We aim, through these changes, to help ensure that researchers, reviewers, and journal editors are better equipped to improve the rigour and transparency of the scientific process and thus reproducibility.
Aim: To evaluate the anti-oxidant enzymes, lipid peroxidation, lipid profile and liver function in albino rats orally administered tartrazine. Study Design: A total number of 63 female albino rats weighing approximately 0.2 kg were used for this study. The study was divided into two phases, phase 1 which lasted for the first 30 days, comprised of 35 rats, 20 rats were used as test group while 15 rats served as the control group. Phase 2 of the study was for 60 days and 28 rats were used with 16 as test group and 12 as the control. The test groups were orally administered with 7.5 mg/kg of tartrazine (ADI) daily over the specified periods while the control groups were not treated with tartrazine but given only food and water. Place and Duration of Study: The study was carried out in the Methodology: At the end of the study, 5 mls of whole blood specimens was collected by means of cardiac puncture into plain bottles. To obtain the serum, the whole blood samples were allowed to clot and later dislodged and spun at 3500 rpm for 10 minutes. The collected serum specimens were used to analyze SOD, MDA, GPX, ALT, GGT, ALP, TG, TCHOL, and HDL-C, while LDL-C was calculated using Friedwald equation. Results: The chronic treatment of rats with tartrazine azo food dye at the ADI dose caused an increase in MDA levels after 30 and 60 days test rats compared to the control, while TCHOL and HDL-C showed significant decrease after 30 and 60 days of treatment in the test group compared to the control group. In addition, ALT indicated significant increase in test group after 60 days of treatment compared to control group. ALP, GGT, TG, LDL-C, SOD and GPX showed no significant difference after 30, and 60 days of treatment at ADI doses. Histologic examination of the liver indicated hydropic dilation, degenerating hepatocyes and infiltration of central vein with parenchymal materials alongside kupffer cells. Conclusion: The results from this study revealed that orally administered tartrazine at the recommended ADI dose increased lipid peroxidation as seen in the elevated MDA levels. Hepatic derangements were also seen as revealed by increased ALT and histologic distortions as well fall in TCHOL and HDL-C lipid fractions.
Erythrosine and tartrazine are common artificial food additives which have become a part of daily human consumption. Advised daily intake values for these agents are set strictly, however, the actual intake is much higher than the recommended ADI. A higher intake of erythrosine and tartrazine is shown to exhibit adverse effects in mammalian models, and is thus a matter of public health concern. In this study we have assessed and compared the dose-dependent effects of erythrosine and tartrazine on inducing oxidative stress in zebrafish embryos. We performed the superoxide dismutase (SOD) enzyme activity assay to test the effect of the two food colorants on reactive oxygen species (ROS) production. Erythrosine and tartrazine treated embryos showed significantly increased SOD activity in an enzyme assay. Additionally SOD mRNA transcripts in the treated embryos were found to be upregulated. Erythrosine and tartrazine treatment specifically altered SOD1 mRNA transcript levels while it had no effect on SOD2 mRNA, the other isoform found in zebrafish. Our study shows that erythrosine at a concentration of 0.05% is embryotoxic in a dose and time dependent manner. Tartrazine treated embryos exhibit similar toxicity at a concentration of 0.5%. Erythrosine treated zebrafish embryos hatch much slower when compared to tartrazine treated embryos and control embryos. While erythrosine affects the yolk utilization, tartrazine exhibits teratogenic effects on early zebrafish embryos. The mRNA expression as well as biochemical analysis indicates that exposure to food colorants induces cytoplasmic SOD transcription to combat the ROS toxicity in zebrafish embryos.
Objective of this study was to investigate the changes of oxidative stress parameters in Chinese hamster ovary (CHO) cells exposed to xanthene food dyes (erythrosine and phloxine), commonly-used azo dyes in the food industry. For this purpose, glutathione (GSH) and malondialdehyde (MDA) levels, glutathione peroxidase (GPx) and catalase (CAT) activity measurements of CHO cells treated with erythrosin (50 µM) and phloxine (40 µM) were compared with the control group. There was no significant difference between MDA levels in CHO cells exposed to both dyes and control group (p > 0.05), however GSH levels significantly decreased with dye addition (p ≤ 0.05). An increase in GPx activity of the CHO cells exposed to phloxin was observed (p ≤ 0.05). However, there was no change in GPX activity of erythrosin-exposed CHO cells (p > 0.05). In terms of CAT activity, difference between the dye-added cells and the control group was not observed. Consequently, decrease in level of GSH, which one of major antioxidant components in the cell, suggests that erythrosine and phloxine can have a toxic effect.
Background:
Tartrazine (Yellow 5 or E102) is a synthetic food dye able to modify perception and behavior, causing agitation, confusion, rhinitis and can produce hyperactivity syndrome in children when is combined with benzoates. Additionally, it can trigger oxidative stress which consequently generates metabolic disorders. Therefore, the study was designed to evaluate the harmful effects of the food additive tartrazine and to observe beneficial properties of blackthorn fruits (Prunus spinosa) on the blood and organs of albino Wistar rats.
Materials and methods:
This study was carried out on 20 mature Wistar rats, randomly divided into four groups of five animals. Over the course of the experiment, the control group received only food and drinking water, group I received 75 mg of tartrazine dissolved in (250 ml) water group II was given 75 mg of tartrazine and 200 mg of dried blackthorn fruit powder 200 mg dissolved simultaneously in (250 ml) of tartrazine-water mixture (aiming to reduce the tartrazine toxicity) and group III received a higher dose of tartrazine (100 mg) in (250 ml) of water.
Results:
At the end of the experiment, values regarding kidney and liver weight were significantly increased, while the weight of the spleen was slightly decreased compared with the weight of the control group. Biochemical and hematological assays, of the blood samples show that the addition of tartrazine in the diet of rats caused significant changes in all biochemical and hematological parameters of the blood. In the group II, which received (P. spinosa) powder combined with tartrazine, the biochemical and hematological parameters had average values similar to the control group.
Conclusions:
Histopathological assay showed that the application of tartrazine in the group I, II and III produced lesions of the kidneys, spleen and the liver for all rodents. Tartrazine was able to generate histopathological changes, which caused significantly tissue lesions of the liver and significant changes in blood parameters. Blackthorn powder showed a promising protective role for the blood parameters but demonstrated no significant benefits for the organs.
Increasing awareness has been lately paid to the toxicity of synthetic additives used in food. The main aim of this study was to survey the renal and testicular toxicity of synthetic food dye brilliant blue. Administration of the BB changed body and relative organs weights, serum creatinine, urea (BUN), uric acid and serum FSH, LH, testosterone levels. This study proved that BB induced oxidative damage as manifested by significant increase in Lipid peroxidation with disorganization in the activity of glutathione peroxidase, protein carbonyl and reactive oxygen species content. Histopathological changes include: infiltration and vacuolation in kidney. In addition; degeneration and necrosis of spermatogoneal cells lining seminiferous tubules in testis. Furthermore; BB induced appotosis via activation of casp-3. Administration of curcumin with BB attenuated the cytotoxic effects of brilliant blue on kidney and testis tissues and reducing apoptotic cell death as well as improved the redox status of kidney and testis. Keywords: Brilliant blue dye, Curcumin, Kidney, Testis, Histopathology, Rats.
Colouring agents are highly present in diverse products in the human environment. We aimed to elucidate the fibrogenic cascade triggered by the food dyes tartrazine and chlorophyll. Rats were orally given distilled water, tenfold of the acceptable daily intake of tartrazine, or chlorophyll for 90 consecutive days. Tartrazine-treated rats displayed a significant rise (p < 0.05) in the mRNA levels and immunohistochemical localization of the renal and hepatic fibrotic markers collagen 1-α, TGFβ-1, and fibronectin and the apoptotic marker caspase-3. Moreover, a significant increment (p < 0.05) in the levels of AST, ALP, creatinine, and urea was evident in both experimental groups but more significant differences were noticed in the tartrazine group. Furthermore, we found a marked increment in the MDA level and significant declines (p < 0.05) in the levels of the SOD, CAT, and GSH enzymes in the kidney and liver from tartrazine-treated rats. The histological investigation reinforced the aforementioned data, revealing hepatocytes with fibrous connective tissue proliferation, apoptotic hepatocytes and periportal fibrosis with tubular necrosis, and shrunken glomeruli and interstitial fibrous tissue proliferation. We concluded that, even at the exposure to high concentrations for long durations, chlorophyll exhibited a lower propensity to induce fibrosis, apoptosis, and histopathological perturbations than tartrazine.
Metabolic syndrome is an agglomeration of disorders including obesity, diabetes and cardiovascular diseases and characterized as chronic mild inflammation which elevates the circulatory inflammatory markers. This could be due to mitochondrial dysfunction, oxidative stress and hypoxia as a consequence of high fat diet (HFD) intake. The present study focuses on the effects of HFD on lactate and mitochondrial metabolism as well as tissue dependent changes in glucose transporter (GLUT) expression in liver, skeletal muscles and adipose tissue of mouse. Lactate dehydrogenase (LDH) and mitochondrial dysfunction established the link between the occurrences of metabolic stress due to HFD. In this work, it was observed that chronic HFD administration aggravated the metabolic alterations by causing reduced ATP production, imbalanced oxidative stress and altered class 1 GLUTs expression. Chronic HFD significantly reduced (p < 0.001) the superoxide dismutase (SOD), catalase (CAT) activities alongside elevated liver injury markers AST and ALT. This in turn causes decreased ATP/ADP ratio, mitochondrial dysfunction and exacerbated LDH levels. This imbalance further led to altered GLUT expression in hepatic cells, adipose tissue and skeletal muscles. HFD significantly (p < 0.001) upregulated the GLUT 1 and 3 expressions while significant downregulated (p < 0.001) GLUT 2 and 4 expression in liver, skeletal muscles and white adipose tissue. These results revealed the link between class 1 GLUTs, mitochondrial dysfunction and HFD-induced metabolic disorder. It can be concluded that HFD impacts mitochondrial metabolism and reprograms tissue-dependent glucose transporter.
This study was conducted to evaluate the toxic effects of an azo dye carmoisine widely used in foods and to investigate its relation to carcinogenicity. Carmoisine administered into mice orally in four different doses as control, low, medium, and high equivalent to 0, 4, 200, and 400 mg/kg bw, respectively, for 120 days. The key toxicological endpoint was observed including animal body weight, organ weights, hematology, biochemistry, and molecular biology assessment. The body weights of medium‐ and high‐dose carmoisine‐treated mice group were significantly decreased as compared to the control mice group. Platelet, white blood cell and monocyte counts of treated group were considerably higher, while Hb and red blood cell counts were drastically lower than the control group. The biochemical parameters such as serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, globulin, urea, and creatinine level were significantly increased, while serum cholesterol level was decreased after treatment as compared to the control. RT‐PCR results showed that expression of Bcl‐x and PARP gene was intensively increased, whereas expression of p⁵³ gene was decreased in the mouse liver tissues treated with carmoisine. This study revealed that high‐dose (400 mg/kg bw) treatment of carmoisine was attributable to renal failure and hepatotoxicity. It also would be suspected as a culprit for liver oncogenesis.
Background:
Depression is a common and widespread mood disorder, which affects an emotional level that varies widely in its intensity. Biochemical parameter alterations have been observed in different depression types. In the present study, we examined acetylcholinesterase (AChE), paraoxonase 1 (PON1), and copper levels in moderately-depressed patients and healthy controls to ascertain whether the measurement of red blood cell (RBC) AChE, and plasma PON1 and copper could be used to evaluate moderate depression.
Methods:
This case control study was performed in the Department of Biochemistry, Kasturba Medical College, Manipal Academy of Higher Education, Manipal, Karnataka, India. Patients who met ICD 10 diagnostic criteria were considered as cases. Goldberg's General Health Questionnaire 28 (GHQ-28) was used to select controls. Four ml of blood was collected from 24 cases and 20 controls aged 35-70 years and used to determine RBC AChE, and plasma PON1 and copper levels.
Results:
Red blood cell AChE, and plasma PON1 and copper levels were significantly greater in patients with moderate depression than in controls. Further, a receiver operating characteristic curve for validity of the biochemical parameters in plasma from patients with moderate depression indicated sensitivity and specificity above 85% for copper and PON1.
Conclusion:
Red blood cell AChE, plasma PON1, and copper levels may have roles in the pathogenesis of depressive disorders.
The ability of Rhizopus arrhizus biomass for the removal of dye erythrosine B from aqueous solution was explored. The dye removal capacity of the biomass was evaluated by conducting batch tests using various parameters, viz. effect of pH, biomass dosage, contact time, modified biomasses and initial dye concentrations. The adsorption process followed a pseudo-second-order kinetic model suggesting chemisorption might be the rate-limiting step. The equilibrium process was found to be in good agreement with Langmuir adsorption isotherm, and maximum adsorption capacities of 355.9 mg/g and 363.6 mg/g were achieved with both waste and acid-treated fresh biomass, respectively.
Graphical abstract
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The xanthene class of Erythrosine B (ErB) is a well-recognized color additive that has been used in drugs, foods and cosmetics. ErB is described as inhibitors of protein–protein interaction and is toxic to reproductive and developmental processes. However, the available toxicological information was inconclusive to access the potential risk of ErB to aquatic and other living organisms. Hence, in this study, we investigated the toxicological impacts of ErB by utilizing zebrafish embryos as model organisms. The developmental deformities including survival, hatching, heart rate, malformation and histological changes were evaluated at specific time intervals (12, 24, 36, 48, 60, 72, 84 and 96 hpf), and the oxidative stress markers [catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST) and glutathione peroxidase (GPx)] were also measured to ascertain the relationship between ErB and reactive oxygen species (ROS). The results depict that ErB was found to exert a concentration-dependent (1, 10, 50, 100, 1000 g mL−1) toxicity to zebrafish embryos by reducing the survival (45.3 ± 11.7%), hatching (45 ± 11.12%) and heart rate (49.4 ± 5.2% at 60 hpf) along with significantly induced malformation at 96 hpf. Moreover, the activities of antioxidant enzyme levels (CAT, SOD, GST and GPx) were significantly (P < 0.05) reduced in ErB at 1000 µg mL−1 exposed embryos which clearly stating the generation of ROS by ErB. Similarly, morphology and histological patterns further validate that ErB was found to induce severe abnormalities to zebrafish embryos and/or larvae in a dose-dependent manner. Hence, our preliminary findings show the evidence on the toxicological impacts of food additive ErB against developmental stages of zebrafish embryos through its ROS-mediated pro-oxidant effects.
The present study assessed the long-term daily administration of benzoic acid (BA), potassium sorbate (PS), chlorophyll (CPL), tartrazine (TAZ), and butylated hydroxyanisole (BHA) on hepato-renal changes and DNA damage in rats. Animals were orally administered with the 10 times of the acceptable daily intake (ADI) from each tested substance daily for 60 consecutive days. Blood, liver, and kidney samples were collected to evaluate hematological, biochemical, histopathological, and genotoxic alterations. The extent of liver and kidney damage was evaluated by comet assay and histopathologically. Significant reduction of leukocyte numbers and lymphocytes % in CPL- and TAZ-treated rats. However, significant increases in platelet count in all treated groups after 60 days were detected. The levels of serum transaminases enzymes (ALT, AST), alkaline phosphatase (ALP), and creatinine were significantly increased in all treatments except with BHA group, but no substantial differences were found in urea after 60 days. Aside from BHA, results of DNA damage revealed significant increases in tailed nuclei, tail moment, DNA% in the tail, and tail length in liver and kidney at different degrees. Moreover, the histopathological figures of liver and kidneys affirmed destructive and degenerative changes. The study indicates that most of the tested food additives may provoke genotoxicity and hepato-nephropathy, which could be serious for human health. Therefore, it is necessary to be informed about the hazardous effects of food additives and more attention should be focused towards using natural substitutes.
This study was carried out to assess some kidney function indices in Wistar rats administered ethanol stem extract of Denettia tripetala. The parameters assessed were creatinine, urea, and electrolytes (sodium, potassium, chloride, bicarbonate). Thirty-two albino Wistar rats divided into 4 groups of eight rats each were used in this study. Group 1 was the control group, group II received an oral dose of 100 mg/kg, ethanol stem extract of Denettia tripetala daily, group III received an oral dose of 200 mg/kg ethanol stem extract of Dennettia tripetala daily while group IV received an oral dose of 300 mg/kg ethanol stem extract of Dennettia tripetala daily. After 21 days of treatment the rats were sacrificed and standard analytical methods were used to assay the biochemical parameters. The result of creatinine (mol/L) showed a significant (P<0.05) increase in the treatment groups (9.18 ± 1.22, 12.42 ± 0.87, 14.56 ± 1.46) compared to the control (4.21 ± 0.65) while urea (mol/L) showed significant (P<0.05) decrease in group III and IV (2.76 ± 1.12, 1.61 ± 0.92) compared to the control (6.34 ± 0.25). The electrolytes (Na+ and Cl-) showed significant (P<0.05) increase in the treatment groups compared to the control while K+ (mmol/L) was not significant (p>0.05) compared to the control. However, bicarbonate (mmol/L) showed a significant (P<0.05) decrease in group II and group III compared to the control. The result of this study has shown that administration of ethanol stem extract of Dennettia tripetala may induce toxicity to the kidney which may hamper renal function.
This study aimed to evaluate the protective role of Nigella sativa oil against the adverse effects of tartrazine on male rats. 18 albino rats were divided randomly into four groups (n = 6). The first (G1) is the negative control, the second group (G2) is the positive control received 10 mg/kg b.w. tartrazine in the diet and the third (G3) received the same dose of tartrazine as in G2 and co-treated with Nigella sativa oil for 8 weeks. Tartrazine decreased total protein, antioxidants and high density lipoproteins, whereas increased liver enzyme, kidney function parameters, total cholesterol, triglycerides, low density lipoproteins and lipid peroxidation in the positive control group. In addition, it caused pathological changes in the tissues of liver, kidney, testes and stomach. Treating tartrazine supplemented rats of G3 with Nigella sativa oil for 8 weeks significantly improved all biochemical parameters and restored the tissues of kidney, stomach, testes and liver to normal. It could be concluded that N. sativa oil succeeded in protecting male rats against the adverse conditions resulted from tartrazine administration.
Tartrazine is a synthetic organic azo dye widely used in food and pharmaceutical products. The current study aimed to evaluate the possible adverse effect of this coloring food additive on renal and hepatic structures and functions. Also, the genotoxic potential of tartrazine on white blood cells was investigated using comet assay. Twenty adult male Wistar rats were grouped into two groups of 10 each, control- and tartrazine-treated groups. The control group was administered orally with water alone. The experimental group was administered orally with tartrazine (7.5 mg/kg, b.wt.). Our results showed a marked increase in the levels of ALT, AST, ALP, urea, uric acid, creatinine, MDA and NO, and a decreased level of total antioxidants in the serum of rats dosed with tartrazine compared to controls. On the other hand, administration of tartrazine was associated with severe histopathological and cellular alterations of rat liver and kidney tissues and induced DNA damage in leucocytes as detected by comet assay. Taken together, the results showed that tartrazine intake may lead to adverse health effects.
Objective:
Certain dietary constituents can induce toxicity and play a critical role in the development of several hepatic disorders. Tartrazine, metanil yellow and sunset yellow are widely used azo dyes in food products, so the present study is aimed to investigate the food color induced hepatotoxicity in Swiss albino rats.
Materials and methods:
Swiss albino rats were divided into four groups, each group having six animals. Group I served as control, Group II, Group III and Group IV were administered with 25, 50 and 75 mg/kg body weight blend of sunset yellow, metanil yellow and tartrazine for 30 days. Hepatotoxicity in rats treated with a blend of these food colors was studied by assessing parameters such as serum total protein, serum albumin, serum alkaline phosphatase (ALP) as well as hepatic malondialdehyde (MDA). The activity of superoxide dismutase (SOD), reduced glutathione (GSH) and catalase (CAT) were assessed.
Results:
Significantly increased concentrations of serum total protein, serum albumin, serum ALP and hepatic MDA and significantly lowered levels of SOD, reduced GSH and CAT in the liver tissue of treated animals were observed when compared with control animals. The alteration in the liver includes necrosis of hepatocytes, infiltration and vacuolation.
Conclusion:
The result indicates that consumption of food color in diet induces liver tissue damage. The used doses of food color were mostly attributable to hepatocellular damage and drastic alteration in antioxidant defense system.
The scenario of usage of synthetic food colours in India is changing. Till recently, eight synthetic dyes were permitted to be added to specified food items at the maximum level of 200 ppm. Widespread prevalence of fraudulent practices like use of unpermitted colours or misuse of permitted colours and the inherent toxicity of these dyes has led the authorities to revise the regulatory provisions and make the laws pertaining to use of synthetic food colours more stringent. To fulfil the ultimate goal of reducing the total exposure to colours, data on dietary intake of food colours needs to be generated urgently in the country. Meanwhile, as the manufacturers are adding colour to food products to improve the appearance and consumer appeal, the consumers can play an important role in reducing their exposure to food colours by demanding foodstuffs free of artificial colour.
The following study is about Tartrazine (E 102) which is known as an azo dye used in food products, drugs and cosmetics. As a part of the safety assessment of Tartrazine, a 13‐week subchronic oral toxicity study was performed on Wistar rats of both sexes. The animals were divided into 5 groups of 6 animals each, 3 of each sex, and fed a diet containing 5, 7.5, or 10 mg/kg b.w, of Tartrazine and 3.75 mg/kg b.w, of Sulfanilic acid. There were no treatment‐related adverse effects with regard to body weight, food and water consumption. Their blood samples were analyzed for hematological measurements, Glucose, Creatinine, Blood urea nitrogen, Cholesterol total, Triglecerid, alanine aminotransferase, aspartate aminotransferase. The Stomach, Jejunum, Liver, Kidneys tissues were also processed for histological examination. The present study shows that Tartrazine and Sulfanilic acid induced a morphological change from the discoid shape to an echinocytic form in rat RBCs. Relative weights of the liver were significantly increased in group treated with 10 mg/kg b.w, of Tartrazine. Our data showed a significant increase in GLU, CREA, CHOL, TG, AST, and total Protein in serum of rats treated with Tartrazine and Sulfanilic acid compared to control rats and these significant changes were more apparent in high doses than low ones. The histopathological changes of Liver and Kidney were in accordance with the biochemical findings.
Food additives were known since the old man from the ancient civilizations to introduce special color or taste in his food. Nowadays, there are over-use of synthetic chemicals as food additives to preserve foods, to improve characters and attract consumers especially children. Previous studies had reported many effects of overdoses from food additives, however, further scientific studies are needed in the molecular levels. The current work studied the effects of doses equivalent to the acceptable daily intake (ADI), 5 and 10 ADI folds of the synthetic food color (Carmoisine) on the experimental animals (male albino rats) for different periods. Gene expression of some fuel metabolism genes e.g. PPAR-alfa, ACo-A and CPT-1 were studied and supported by histological studies on rat liver. There were down-regulations of the studied genes which may leads to the conclusion that, carmoisine may decrease the fuel metabolism. The histological studies indicate also that high doses of carmoisine may affect the liver.
In this study, different concentrations of five food dyes (amaranth, patent blue, carminic acid, indigotine and erythrosine) have been evaluated for genotoxicity in the Somatic Mutation and Recombination Test (SMART) of Drosophila melanogaster. Standard cross was used in the experiment. Larvae including two linked recessive wing hair mutations were chronically fed at different concentrations of the test compounds in standard Drosophila Instant Medium. Feeding ended with pupation of the surviving larvae. Wings of the emerging adult flies were scored for the presence of spots of mutant cells which can result from either somatic mutation or somatic recombination. For the evaluation of genotoxic effects, the frequencies of spots per wing in the treated series were compared to the control group, which was distilled water. The present study shows that carminic acid and indigotine demonstrated negative results while erythrosine demonstrated inconclusive results. In addition 25 mg mL(-1) concentration of patent blue and 12.5, 25 and 50 mg mL(-1) concentrations of amaranth demonstrated positive results in the SMART.
Erythrosine, a synthetic red dye widely used in food products, has been linked to potential health risks, raising concerns about its safety. This study aimed to evaluate the subacute toxicity of the synthetic food dye erythrosine in the brains of Wistar rats. Twenty‐four 6‐ to 7‐week‐old female rats were randomly divided into four groups of six ( n = 6); the control group and the other three groups, which were established on the basis of erythrosine's acceptable daily intake (ADI, 0.1 mg per kg body weight); 1/4 ADI, 1/2 ADI, and ADI; for 28 days. Significant alterations in the enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione‐S‐transferase (GST), and acetylcholinesterase (AchE) were observed at all erythrosine dosages, with a substantial decline at ADI dosages ( p ≤ 0.05). Increased oxidative stress markers, viz., malondialdehyde content and lactate dehydrogenase activity, were observed in ADI‐administered rats. The H 2 O 2 content decreased at 1/4 ADI and 1/2 ADI dosages and thereafter increased with increasing dosage. The comet assay demonstrated that the ADI dosage for 28 days resulted in the most significant damage, as evidenced by the increased tail length, tail DNA percentage, and tail moment. Light microscopy revealed various anomalies in brain histology, such as atrophies, vacuolization, shrunken cells, pyknotic nuclei, and reduced cell density. The results of the present study demonstrated that erythrosine disrupts the normal histopathology of the brain, suppresses antioxidative and acetylcholinesterase enzymatic activity, and increases lipid peroxidation and DNA damage, thereby resulting in erythrosine toxicity even at doses lower than the ADI.
Erythrosine, a synthetic food dye, has been controversial due to its potential health risks. This study examines the effect of erythrosine on activity of antioxidative enzymes, oxidative stress indices, DNA damage through comet assay, and histopathological changes on stomach, intestine, and colon over a period of 28 days in rats. Twenty‐four rats were randomly divided into four groups ( n = 6). The first is the control group and then one each for three doses of erythrosine based on acceptable daily intake (¼ ADI, ½ ADI, and ADI, 0.1 mg/kg body weight). The results revealed that with increasing dosages the activity of catalase decreased in stomach and intestine but in colon, the catalase activity increased. Superoxide dismutase and glutathione‐S‐transferase activity decreased in dose‐dependent manner in all three tissues. While, in stomach and intestine, the acetylcholinesterase activity showed increment in ¼ ADI dose group and then declined in ½ ADI and ADI dose‐administered rats. The oxidative stress indicators showed elevated levels of lipid peroxidation, hydrogen peroxide concentration, and lactate dehydrogenase activity suggesting heightened free radical activity and potential oxidative damage. The comet test was used to evaluate DNA damage, revealing substantial damage in the erythrosine administered groups. Histopathological examination showed inflammatory infiltration and other degenerative changes in gastrointestinal tract, highlighting the dye's adverse effects. The research underscores the need for a comprehensive reevaluation of the safety and toxicity of food dyes like erythrosine, especially considering the inconsistencies in existing studies regarding the dye's safety.
25 male Wistar rats (140-170g) were partitioned into 5 groups (n = 5). 2.5mg/kg, 5mg/kg, 10mg/kg and 20mg/kg of combine Tartrazine and Erythrosine (T + E; 50:50) were administered for 23 days. Serum urea and creatinine, gene expression and profiling of pro-inflammatory cytokine (Tumor Necrosis Factor- α gene), Caspase-9 and Kidney injury molecule-1 (KIM-1) and histomorphological examination of the kidney were investigated. The fold change of relative gene expression of TNF-α gene showed significantly (p < 0.05) up-regulation in all the treated rats except for the 10mg/kg T + E treated rats when compared to control rats. Casp-9 and KIM-1 genes were significantly (p < 0.05) up-regulated in low dose treatment (2.5mg/kg T + E and 5mg/kg T + E) and down-regulated in high dose treatment (10mg/kg T + E and 20mg/kg T + E). However, there was significant (p < 0.05) increase in serum urea concentration in the rats treated with 5mg/kg T + E and 20mg/kg T + E while the rats treated with 10mg/kg T + E indicated a significant (p < 0.05) decrease. Conversely, serum creatinine concentration indicated significant (P < 0.05) increase in10mg/kg T + E and 20mg/kg T + E treated rats versus the control. From the histomorphological examination of the kidney, there was hypertrophy of the glomeruli in relation to the size of Bowman's capsule in the 10mg/kg T + E and 20mg/kg T + E treated rats. Kidney function was impaired as evident in up-regulation of TNF-α gene, KIM-1 gene, and serum urea and creatinine concentration with down-regulation of Casp-9 gene. The combined treatment also tampers with the architecture of the kidney.
Metanil yellow, an azo dye, is a non-permitted synthetic food colour used extensively in India and other developing countries as food additive. Present communication reports the toxic effects of metanil yellow on hepatic and kidney tissues and its amelioration by eugenol, vitamin E and vitamin C. Oral administration of metanil yellow in albino Wistar rats for 28 days caused elevation in serum enzymes (glutamate oxaloacetate transaminase, gluatamate pyruvate transaminase, alkaline phosphatase), and total bilirubin along with decline in albumin and total protein levels. At tissue level, activities of oxidative stress markers viz., superoxide dismutase, catalase and reduced glutathione in liver and kidney were reduced to about half while malondialdehyde level increased significantly under the influence of metanil yellow. Co-administration of eugenol/vitamin E/vitamin C in metanil yellow intoxicated rats exhibited considerable restoration of oxidative stress as well as hepatic and renal function markers in serum and tissues. The study revealed that eugenol has antioxidant, hepatoprotective and renoprotective activities.
Tartrazine is a synthetic lemon yellow azo dye primarily used as a food coloring. The present study aimed to screen the neurobiochemical effects of Tartrazine in Wistar rats after administering the Acceptable Daily Intake (ADI) level. Tartrazine (7.5 mg/kg b.w.) was administered to 21 day old weanling rats through oral gavage once daily for 40 consecutive days. On 41st day, the animals were sacrificed and brain sub regions namely, frontal cortex, corpus striatum, hippocampus and cerebellum were used to determine activities of anti-oxidant enzymes viz. Superoxide Dismutase (SOD), Catalase (CAT), Glutathione-Stransferase (GST), Glutathione Reductase (GR) and Glutathione Peroxidase (GPx) and levels of lipid peroxides using Thio-barbituric Acid Reactive Substance (TBARS) assay. Our investigation showed a significant decrease in SOD and CAT activity, whereas there occurred a decline in GST and GR activity with an increase in GPx activity to counteract the oxidative damage caused by significantly increased levels of lipid peroxides. The possible mechanism of this oxidative damage might be attributed to the production of sulphanilc acid as a metabolite in azofission of tartrazine. It may be concluded that the ADI levels of food azo dyes adversely affect and alter biochemical markers of brain tissue and cause oxidative damage.
The liver is the largest internal organ in the human body and it is the main site for the metabolism of endogenous molecules and xenobiotics. Drug-induced liver injury is one of the leading causes of drug attrition during drug development and post-marketing drug withdrawal. Current biomarkers can detect liver injury but there are many inadequacies that make them less than ideal. For example, the serum level of alanine aminotransferase (ALT) is the most commonly used biomarker of hepatocellular injury, but its elevation can also reflect muscle injury. Therefore, more sensitive and specific biomarkers are needed to better predict liver toxicity. The omics technologies including genomics, proteomics, and metabolomics have been employed in hepatotoxicity studies to identify new biomarkers. This chapter evaluates the existing and emerging hepatotoxicity biomarkers from the omics platforms as well as from analysis of microRNAs in human body fluids. A brief description of the qualification of biomarker candidates is also given.
Food colours are added to different types of commodities to increase their visual attractiveness or to compensate for natural colour variations. The use of these additives is strictly regulated in the European Union, the United States and many other countries worldwide. There is a growing concern about the safety of some commonly used legal food colourants and there is a trend to replace the synthetic forms with natural products. Additionally, a number of dyes with known or suspected genotoxic or carcinogenic properties have been shown to be added illegally to foods. Robust monitoring programs based on reliable detection methods are required to assure the food is free from harmful colours. The aim of this review is to present an up to date status of the various concerns arising from use of colour additives in food. The most important food safety concerns in the field of food colours are lack of uniform regulation concerning legal food colours worldwide, possible link of artificial colours to hyperactive behaviour, replacement of synthetic colours with natural ones and the presence of harmful illegal dyes - both known but also new, emerging ones in food. The legal status of food colour additives in the EU, US and worldwide is summarized. The reported negative health effects of both legal and illegal colours are presented. The European Rapid Alert System for Food and Feed notifications and US import alerts concerning food colours are analyzed and trends in fraudulent use of colour additives identified. The detection methods for synthetic colours are also reviewed.
Food additives are used for various purposes, including preservation, colouring and sweetening. Some food additives, however, have been prohibited from use because of their toxicity. Azo dyes are one of these food additives which widely used as colorants in foods. The extent of such use is related to the degree of industrialization of the society. Approximately 1-5× 10 5 pounds of the dye amaranth were used each year in over 60countries. The present study aimed to investigate the possible influence impacts of amaranth (red dye) on some hematological and biochemical parameters of male albino rat, Rattus norvegicus . So, sixty adult male rats weighing 100-110gm. were divided into 3groups, the first one served as a control, the second received 25mg/kg of amaranth and the third group was treated with 75mg/kg of amaranth. Rats were treated orally for 30days followed a recovery for another 30days. The obtained data reveal a marked decrease in the percentage of body weight gain, red blood cells (R.B.Cs) counts, Hemoglobin (Hb) content, mean corpuscular hemoglobin concentration (MCHC), serum total lipids and serum total cholesterol of rats treated with the high dose of amaranth. On the other hand, a noticeable increase in hematocrit (Hct) value, Mean corpuscular volume (MCV), activities of Serum aspartate aminotransferase (AST) , alanine aminotransferase (ALT), alkaline phosphatase (ALP), glucose level, serum total protein and globulin were found in rats treated with the high dose of amaranth. In general, there was appreciable improvement after the recovery period.
In food industry there are used substances from azoic dyes such as carmoisine and tartrazine. Therefore we decided to verify by a histological study, the effect of these two dyes, administered in drinking water in concentrations of 1, 2 and 3% for 3 weeks, on liver and kidney in guinea pigs. At the end of the experiment animals were euthanized and pieces of liver and kidneys were collected and histologically processed through inclusion in paraffin. For both liver and kidney we observed phenomena represented by stasis and oedema, congestion, hepatocyte and kidney apoptosis, with atrophy of renal corpuscles. Magnitude and severity of histopathological aspects observed were directly proportional to the concentration of the administered dyes.
The effect of simulated acid rain (AR) (pH 1.8) on H2O2 and malonyldialdehyde (MDA) levels and activities of peroxidase and catalase in bean plants were investigated. The influence of exogenous polyamines spermidine and spermine on these parameters was also studied. AR treatment induced lipid peroxidation and increased level of H2O2 in leaves. Pretreatment with spermidine and spermine prevented these changes. The protective effect of spermine was higher than that of spermidine. The impact of polyamines could be attributed to their acid neutralizing and antioxidant effects, as well as to their ability to stabilize membranes by associating with negatively charged phospholipids. It was also found that AR significantly increased peroxidase and decreased catalase activities at the first hours after treatment. Later, both enzyme activities were enhanced that could contribute to the scavenging and detoxification of active oxygen species.
Xenobiotics, which are absorbed into biological systems by passive diffusion across membranes are usually lipid soluble and not ideally suited for excretion. Indeed very lipophilic substances may remain in the mammalian body for many years. After a xenobiotic has been absorbed, it may undergo biotransformation to products which are rapidly excreted and therefore elimination of the compound from the animal is facilitated. However, biotransformation may also change the biological activity of the substance. Hence, the metabolic fate of the compound can have an important bearing on its toxic potential, the disposition of the compound in the body and the excretion of the compound. The metabolic reactions involved are usually divided into phase 1 and phase 2 reactions, the latter being conjugation reactions. The products of metabolism are usually more water soluble than the original compound. Although usually detoxifying, these reactions, especially phase 1 ones, sometimes increase toxicity.
Keywords:
biotransformation;
metabolism;
Phase 1;
Phase 2;
conjugation;
cytochrome;
hydroxylation;
oxidation;
dealkylation
A photometric method for determining acetylcholinesterase activity of tissue extracts, homogenates, cell suspensions, etc., has been described. The enzyme activity is measured by following the increase of yellow color produced from thiocholine when it reacts with dithiobisnitrobenzoate ion. It is based on coupling of these reactions: The latter reaction is rapid and the assay is sensitive (i.e. a 10 μ1 sample of blood is adequate). The use of a recorder has been most helpful, but is not essential. The method has been used to study the enzyme in human erythrocytes and homogenates of rat brain, kidney, lungs, liver and muscle tissue. Kinetic constants determined by this system for erythrocyte eholinesterase are presented. The data obtained with acetylthiocholine as substrate are similar to those with acetylcholine.
Heavy metals are known to reduce the activities of antioxidant enzymes (e.g. superoxide dismutase, catalase), while organophosphorous insecticides are known to inhibit the activity of the enzyme acetylcholinesterase. In this study, the activities of these three enzymes in zebrafish (Danio rerio) tissues were assessed to evaluate the consequences heavy metal and organophosphate contamination in aquatic systems. When the fish were contacted with water containing a single pollutant, superoxide dismutase activity was affected by the presence of Cd but not by methyl parathion or Zn. However, catalase and acetylcholinesterase activities were sensitive to all three pollutants. The combined treatment showed that the three enzymes could be chosen as biomarkers of joint pollution by both metals and organophosphate. Toxicity tests showed an antagonism interaction between methyl parathion and Cd or Zn, and the change of enzyme activities at 96 hours was in accordance with that.
The objective of the present work was to evaluate the broadest toxic effect of some synthetic additives of colorants and/or flavors on different body organs and metabolic aspects in rats. A number of chemical food color and flavor additives are routinely added during processing to improve the aesthetic appearance of the dietary items. However, many of them are toxic after prolonged use. In this experiment, a total of 100 male albino rats of Spargue Dawley strain were divided into 10 groups: G(1) was fed basal diet and served as control, G(2): basal diet + Brilliant blue (blue dye, No. 2, 124 mg/kg diet), G(3): basal diet + carmoisine (red dye, No. 3, 70 mg/kg diet), G(4): basal diet + tartrazine (yellow dye, FD & C yellow No. 5, 75 mg/kg diet), G(5): basal diet + trans-anethole (4.5 g/kg diet) G(6): basal diet + propylene glycol (0.25 g/kg diet), G(7): basal diet + vanillin(1.25 g/kg diet), G(8): basal diet + Brilliant blue + propylene glycol, G(9): basal diet + carmoisine + trans-anethole, G(10): basal diet + tartrazine + vanillin for 42 successive days. All food colorants mixed with or without flavor additives induced a significant decrease in body weight, hemoglobin concentration and red blood cell count. Also there was a significant decrease in reduced glutathione content; glutathione-S-transferase and superoxide dismutase activities in both blood and liver compared to control group. On the other hand, a significant increase in serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase activities, bilirubin, urea, creatinine, total protein and albumin were observed in all test groups when compared to control group. Finally, it is advisable to limit the uses of these food colorants and/or food flavor additives especially those used by children.
The effects of 7 days' exposure to differing Triclosan (TCS) concentrations (300, 600, and 900 ng/L) were investigated in the clam Ruditapes philippinarum. Vitellogenin (Vg)-like protein levels in haemolymph and digestive gland from males and females, gill acetylcholinesterase (AChE) activity, superoxide dismutase (SOD) and catalase (CAT) activities in gills and digestive gland, and gill lipid peroxidation (LPO) were measured. The highest TCS concentrations decreased significantly Vg levels in male haemolymph and digestive gland, whereas no significant variations were found in females. The highest TCS concentrations increased significantly SOD activity in gills, but decreased it in digestive gland. No changes in CAT activity were observed. In gills, TCS reduced significantly AChE activity, but it did not induce significant variations in LPO. Our study demonstrates that TCS alters biochemical parameters in R. philippinarum, even at environmentally realistic concentrations, and suggests differing modes of action of the contaminant, in clams at least.
Three different synthetic chocolate colourant agents (A, B and C) were administered to healthy adult male albino rats for 30 and 60 day periods to evaluate their effects on body weight, blood picture, liver and kidney functions, blood glucose, serum and liver lipids, liver nucleic acids (DNA and RNA), thyroid hormones (T3 and T4) and growth hormone. In addition, histopathological examinations of liver, kidney and stomach sections were studied. These parameters were also investigated 30 days after colourant stoppage (post effect). Ingestion of colourant C (brown HT and indigocarmine) significantly decreased rat body weight, serum cholesterol and HDL-cholesterol fraction, while, T4 hormone, liver RNA content, liver enzymes (S. GOT, S. GPT and alkaline phosphatase), total protein and globulin fractions were significantly elevated. Significant increases were observed in serum total lipids, cholesterol, triglycerides, total protein, globulin and serum transaminases in rats whose diets were supplemented with chocolate colours A and B (sunset yellow, tartrazine, carmoisine and brilliant blue in varying concentrations). Haematological investigations demonstrated selective neutropenia and lymphocytosis with no significant alterations of total white blood cell counts in all rat groups, while haemoglobin concentrations and red blood cell counts were significantly decreased in the rats who were administered food additives A and B. Eosinophilia was noted in rats fed on colourant A only. No changes were recorded for blood glucose, growth hormone and kidney function tests. Histopathological studies showed brown pigment deposition in the portal tracts and Van Küpffer cells of the liver as well as in the interstitial tissue and renal tubular cells of the kidney mainly induced by colourant A. Congested blood vessels and areas of haemorrhage in both liver and renal sections were revealed in those rats who were given colourants B and C. There were no-untoward-effects recorded in the stomach tissue.
Tartrazine and carmoisine are an organic azo dyes widely used in food products, drugs and cosmetics. The present study conducted to evaluate the toxic effect of these coloring food additives; on renal, hepatic function, lipid profile, blood glucose, body-weight gain and biomarkers of oxidative stress in tissue. Tartrazine and carmoisine were administered orally in two doses, one low and the other high dose for 30 days followed by serum and tissue sample collection for determination of ALT, AST, ALP, urea, creatinine, total protein, albumin, lipid profile, fasting blood glucose in serum and estimation of GSH, catalase, SOD and MDA in liver tissue in male albino rat. Our data showed a significant increase in ALT, AST, ALP, urea, creatinine total protein and albumin in serum of rats dosed with tartrazine and carmoisine compared to control rats and these significant change were more apparent in high doses than low, GSH, SOD and Catalase were decreased and MDA increased in tissue homogenate in rats consumed high tartrazine and both doses of carmoisine. We concluded that tartrazine and carmoisine affect adversely and alter biochemical markers in vital organs e.g. liver and kidney not only at higher doses but also at low doses.