Comprehensive analysis of metabolic changes in rats exposed to acrylamide

Zhao, Shiyuan; Zhong, Haitao; Geng, Chunmei; Xue, Hongjia; Wang, Changshui; Sun, Wenxue; Dang, Ruili; Han, Wenxiu; Jiang, Pei

doi:10.1016/j.envpol.2021.117591

Cited by 20 publications

(20 citation statements)

References 78 publications

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“…Oxidative stress is one of the main mechanisms explaining the neurotoxicity and hepatotoxicity following ACR exposure [ 28 , 30 ]. Increased ROS production, as a result of ACR exposure, may adversely affect cell survival, due to cell membrane damage by oxidative degradation of lipids, proteins, and irreversible DNA modification [ 21 , 25 , 33 ].…”

Section: Introductionmentioning

confidence: 99%

“…It is abundant in fried and roasted potato, vegetable crisps, cocoa and roasted coffee, bread and pastry, cookies, as well as in tobacco smoke, and, in lower concentrations, in breakfast cereals, biscuits, crackers, roasted nuts, homemade food, human breast milk, infant milk powder and a range of baby foods [21,23,[25][26][27]. ACR can be absorbed through the digestive tract, respiratory system or through the skin and after exposure can be rapidly distributed to many tissues and organs, such as the thymus, thyroid, liver, heart, brain, spleen, kidneys, as well as the human placenta and breast milk [21,25,27,28]. It is further transformed by an enzymatic reaction involving cytochrome P450 2E1 into a more toxic and reactive epoxide, glycidamide, which is widely distributed into the tissues [21,24,26,29].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, oxidative damage is aggravated by decreased antioxidant enzyme activities, such as those of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GPx), which act as free radical traps in conditions associated with oxidative stress [21,25,33,34]. Since both ACR and glycidamide can be conjugated to glutathione (GSH) as a detoxifying pathway of ACR, forming GSH adducts that are subsequently converted to mercapturic acids, which are used as biomarkers of ACR exposure, the consequence is GSH depletion [25,28,29]. Therefore, proteomics studies suggest that ACR-induced toxicity may be mediated by cellular oxidative stress following extensive GSH consumption [25,28].…”

Section: Introductionmentioning

confidence: 99%

“…Since both ACR and glycidamide can be conjugated to glutathione (GSH) as a detoxifying pathway of ACR, forming GSH adducts that are subsequently converted to mercapturic acids, which are used as biomarkers of ACR exposure, the consequence is GSH depletion [25,28,29]. Therefore, proteomics studies suggest that ACR-induced toxicity may be mediated by cellular oxidative stress following extensive GSH consumption [25,28]. Free radicals are produced continuously in vivo and protective antioxidant enzymes (SOD, CAT, GST, GPx), as well as reduced GSH, have roles in coping with these toxic substances [33,35].…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats

et al. 2022

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In recent years, it has been increasingly suggested that the consumption of natural polyphenols, in moderate amounts, is beneficial for health. The aim of this study was to investigate the efficacy of a red wine (the administered dose of 7 mL/kg/day being equivalent to ~16.5 mg/kg/day total polyphenols) compared to a white wine (the administered dose of 7 mL/kg/day being equivalent to ~1.7 mg/kg/day total polyphenols), on the prevention of acrylamide-induced subacute hepatic injury and oxidative stress in Wistar rats. Hepatic damage due to acrylamide intoxication (the administered dose being 250 µg/kg body weight, for 28 days, by intragastric gavage) was assessed by employing biochemical parameters (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and by histopathological studies. Markers of oxidative damage were measured in terms of plasma malondialdehyde (MDA), hepatic Thiobarbituric Acid Reactive Substances (TBARS) and glutathione (GSH) levels, and liver antioxidant enzyme (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) activities. Regarding hepatic enzyme activities, treatment with red wine significantly decreased the AST values (p < 0.05), while for the ALT values only a normalization tendency was observed. Treatment with red wine and white wine, respectively, significantly prevented the increase in MDA and TBARS levels (p < 0.05), as well as the depletion of GSH (p < 0.05). Red wine treatment normalized the activities of the antioxidant enzymes CAT and SOD in rats intoxicated with acrylamide, while supplementing the diet with white wine did not produce significant differences in the antioxidant enzyme activities. Histopathological findings revealed a moderate protective effect of red wine after four weeks of daily consumption. Our findings provide evidence that red wine, having a higher phenolic content than white wine, has a significant protective effect on oxidative stress and liver injury induced by acrylamide in rats, through its antioxidative activity.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats

et al. 2022

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“… 9 It enables a global evaluation of metabolites in biological samples and provides a valuable approach for biomarker identification. 10 , 11 The main types of samples used for metabolomics studies are urine, serum, saliva, liver, and heart. 12 , 13 , 14 , 15 , 16 Alterations in metabolites and disrupted metabolic pathways facilitate elucidating the mechanism of action of disease or treatment.…”

Section: Introductionmentioning

confidence: 99%

Impact of a long‐term high‐fructose diet on systemic metabolic profiles of mice

Wang

Han

et al. 2022

FASEB BioAdvances

Self Cite

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Evidence is mounting that chronic high‐fructose diets (HFrD) can lead to metabolic abnormalities and cause a variety of diseases. However, the underlying mechanism by which long‐term high fructose intake influencing systemic metabolism remains unclarified. This study, therefore, attempted to investigate the impact of a high‐fructose diet on metabolic profile. Four‐week‐old male C57BL/6 mice were fed with 15% fructose solution as their only source of water for 8 weeks. Afterward, gas chromatography–mass spectrometry (GC–MS) was employed to investigate the comprehensive metabolic profile of serum, muscle, liver, heart, white adipose, brain, and kidney tissues, and multivariate analyses including principal component analysis (PCA) and orthogonal partial least squared‐discriminant analysis (OPLS‐DA) were applied to screen for differential metabolite expression between the HFrD and control groups. Furthermore, the MetaboAnalyst 5.0 ( http://www.metaboanalyst.ca ) and Kyoto Encyclopedia of Genes and Genomes database (KEGG; http://www.kegg.jp ) were employed to portray a detailed metabolic network. This study identified 62 metabolites related to HFrD and 10 disturbed metabolic pathways. The results indicated that high fructose intake mainly influenced amino acid metabolism and biosynthesis (glycine, serine, and threonine metabolism; aspartate, and glutamate metabolism; phenylalanine, tyrosine, and tryptophan biosynthesis, and arginine biosynthesis pathways), glutathione metabolism, sphingolipid metabolism, and glyoxylate and dicarboxylate metabolism in serum, whereas these pathways were suppressed in the brain. Starch and sucrose metabolism in muscle was also disrupted. These results elucidate the effects of long‐term high fructose consumption on the metabolic profiles of various tissues and provide new insight for the identification of potential metabolic biomarkers and pathways disrupted by high fructose.

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Possible metabolic effect of acrylamide on biological system

Gupta,

Singh,

Soni

et al. 2023

Food Safety and Health

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Acrylamide (AA) is a chemical agent mostly used in the manufacture of polymers and copolymers. Recently, it has gained attention because of its production in food items prepared at high‐temperature (>120°C) processes, such as frying, toasting, cooking, roasting or baking of high carbohydrate food items. As per the higher exposure of AA, appropriate identification of its toxic effect is necessary. Hepatotoxicity, nephrotoxicity, neurotoxicity, reproductive toxicity, and immunotoxicity of AA have been observed in several studies. AA could also be considered as endocrine‐disrupting chemicals and its exposure leads to many hormonal abnormalities. Nearly one in every four couples of a developing nation suffers from infertility, and AA exposure may be one of the reasons. AA is proven as a potent reproductive toxicant, affecting both male and female reproductive organ functioning. This review summarizes research conducted on the toxicity of AA in various organs.

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Comprehensive analysis of metabolic changes in rats exposed to acrylamide

Cited by 20 publications

References 78 publications

Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats

Protective Effects of Wine Polyphenols on Oxidative Stress and Hepatotoxicity Induced by Acrylamide in Rats

Impact of a long‐term high‐fructose diet on systemic metabolic profiles of mice

Possible metabolic effect of acrylamide on biological system

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