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环境病理学,毒理学和肿瘤学期刊
影响因子: 1.241 5年影响因子: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN 打印: 0731-8898
ISSN 在线: 2162-6537

环境病理学,毒理学和肿瘤学期刊

DOI: 10.1615/JEnvironPatholToxicolOncol.2014010291
pages 167-182

Reversal of Methylmercury-Induced Oxidative Stress, Lipid Peroxidation, and DNA Damage by the Treatment of N-Acetyl Cysteine: A Protective Approach

Deepmala Joshi
Reproductive Biology and Toxicology Laboratory, UNESCO Satellite center of Trace Element Research & School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, India
Mittal Deepak Kumar
Reproductive Biology and Toxicology Laboratory, UNESCO Satellite center of Trace Element Research & School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, India
Shakya Arvind Kumar
Indira Gandhi National Open University, Biochemistry Department, School of Sciences, New Delhi, India
Shukla Sangeeta
Reproductive Biology and Toxicology Laboratory, UNESCO Satellite center of Trace Element Research & School of Studies in Zoology, Jiwaji University, Gwalior, Madhya Pradesh, India

ABSTRACT

This study was designed to evaluate the protective effect of N-acetyl cysteine in reducing methylmercury (MeHg)−induced oxidative stress, lipid peroxidation, DNA damage in liver, kidney, and brain, and their ability to restore altered hepatic, renal, and other biochemical variables. Male Sprague-Dawley rats (150 ± 10 g) were randomly divided into three groups. Group 1 served as the control. Groups 2 and 3 were administered methylmercury (1 mg kg−1 orally, 5 days/week) for 12 weeks, and group 2 served as the experimental control. Group 3 received N-acetyl cysteine (0.6 mg kg−1 intraperitoneally, two days/week) for 12 weeks after methylmercury exposure. Methylmercury exposure caused a significant rise in bilirubin, gamma-glutamyl transpeptidase, protein, triglycerides, cholesterol, urea, creatinine, uric acid, and blood urea nitrogen, with a concomitant decrease in albumin content, reduced glutathione level and acetyl cholinesterase activity, antioxidant enzymes such as glutathione reductase, glutathione peroxidase, glucose-6-phosphate dehydrogenase, and adenosine triphosphatase. However, lipid peroxidation level, metallothionein expression, and DNA damage with increment of tail length were observed after methylmercury intoxication. N-acetyl cysteine, a widely available, nontoxic amino acid derivative, is a promising antioxidant with a wide spectrum of biological functions. The ability of N-acetyl cysteine to enhance mercury excretion and its wide availability in clinical use indicate that it may be an ideal therapeutic agent against methylmercury poisoning.


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