Cadmium-induced neurological disorders: prophylactic role of taurine.
The present study was conducted to investigate whether the conditionally essential amino acid taurine could play any protective role against the potent neurotoxin cadmium (Cd)-induced oxidative impairment in mice brain. Cd administration in the form of CdCl(2 )(at a dose of 4 mg kg(-1) body weight for 3 days, orally) increased the intracellular accumulation of metallic Cd, reactive oxygen species and super oxide radicals. The toxin also augmented the extent of lipid peroxidation, protein carbonylation and the levels of glutathione disulfide. Activities of the antioxidant enzymes and the levels of reduced glutathione as well as total thiols have been significantly decreased due to Cd exposure. In addition, the toxin also caused significant DNA degradation (as evidenced from DNA smearing and diphenylamine reaction). Oral administration of taurine (at a dose of 100 mg kg(-1) body weight for 5 days) was found to be very effective in the prevention of Cd-induced oxidative impairment in the brain tissue of experimental mice. In addition, taurine treatment could also prevent the reduction in the in vivo antioxidant power linearly up to a dose of 100 mg kg(-1) body weight. The preventive role of taurine against Cd-induced cerebral oxidative damage was supported by the observation under scanning electron microscope as well as histological examination of brain segments. To validate the experimental results, a well-known water soluble antioxidant, vitamin C, was used as the positive control in the study. In all, the results suggest that taurine plays a beneficial role against Cd-induced cerebral oxidative stress.
Department of Chemistry, Bose Institute, Kolkata, India.
Mahua
M
Sinha
Prasenjit
P
Manna
Parames C
PC
Sil
D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D019256:Cadmium Chloride / Q000037:antagonists & inhibitors* / Q000493:pharmacokinetics / Q000633:toxicity*; D053938:DNA Fragmentation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008855:Microscopy, Electron, Scanning; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000517:prevention & control*; D009929:Organ Size / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D013654:Taurine / Q000494:pharmacology*
D000975:Antioxidants; D008054:Lipid Peroxides; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D013481:Superoxides; D013654:Taurine; D008315:Malondialdehyde; D005978:Glutathione; D019256:Cadmium Chloride; D001205:Ascorbic Acid