title: Arsenic-induced oxidative cerebral disorders: protection by taurine.
abstract: The present study was conducted to investigate whether the conditionally essential amino acid, taurine, could play any protective role against the potent neurotoxin arsenic (As)-induced oxidative impairment in the rat brain. Administration in the form of NaAsO(2) (at a dose of 10 mg/kg body weight for 2 days, orally), As increased the intracellular accumulation of metallic As, reactive oxygen species, and super oxide radicals. The toxin also augmented the extent of lipid peroxidation, protein carbonylation, and the levels of glutathione disulphide. Activities of the antioxidant enzymes, membrane-bound enzymes, acetylcholinesterase, and the levels of reduced glutathione, as well as total thiols, have been significantly decreased due to As exposure. Oral administration of taurine (at a dose of 100 mg/kg/body weight for 5 days) was found to be very effective in the prevention of As-induced oxidative impairment in the brain tissue of the experimental rats. To validate the experimental results, a well-known water-soluble antioxidant, vitamin C, was used as the positive control in the study. Combining all, results suggest that taurine plays a beneficial role against As-induced cerebral oxidative stress.
authors.affiliation: Department of Chemistry, Bose Institute, Calcutta, West Bengal, India.
authors.forename: Joydeep
authors.initials: J
authors.lastname: Das
authors.forename: Jyotirmoy
authors.initials: J
authors.lastname: Ghosh
authors.forename: Prasenjit
authors.initials: P
authors.lastname: Manna
authors.forename: Mahua
authors.initials: M
authors.lastname: Sinha
authors.forename: Parames C
authors.initials: PC
authors.lastname: Sil
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000601:Amino Acids, Essential; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001151:Arsenic / Q000633:toxicity*; D020261:Arsenic Poisoning / Q000188:drug therapy*; D001205:Ascorbic Acid / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000627:therapeutic use; D005978:Glutathione / Q000378:metabolism*; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D016877:Oxidants / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013654:Taurine / Q000627:therapeutic use*
chemical_list: D000601:Amino Acids, Essential; D000975:Antioxidants; D016166:Free Radical Scavengers; D016877:Oxidants; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D013654:Taurine; D002374:Catalase; D005982:Glutathione Transferase; D000110:Acetylcholinesterase; D000251:Adenosine Triphosphatases; D005978:Glutathione; D001151:Arsenic; D001205:Ascorbic Acid