title: Induction of necrosis in cadmium-induced hepatic oxidative stress and its prevention by the prophylactic properties of taurine.
abstract: The present study has been carried out to investigate the protective role of taurine against cadmium (Cd)-induced oxidative impairment in murine liver. Oral administration of cadmium chloride (CdCl(2)) at a dose of 4mg/kg body weight for 6 days increased the accumulation of the Cd in the liver and diminished the liver weight to body weight ratio. The CdCl(2) altered the levels of intracellular trace elements, cofactors of various metalloenzymes and increased the activities of serum marker enzymes related to liver dysfunction. In addition, Cd intoxication also attenuated intracellular antioxidant power, the activities of antioxidant enzymes as well as the levels of cellular metabolites. Moreover, level of hepatic metallothionein, lipid peroxidation, protein carbonylation, DNA fragmentation, concentration of intracellular reactive oxygen species (ROS) and the activities of cytochrome P450s have been increased due to Cd toxicity. In addition to the oxidative impairments, Cd exposure caused hepatic cell death mainly via the necrotic pathway. Oral administration of taurine at a dose of 100mg/kg body weight for 5 days prior to CdCl(2) intoxication prevented the alterations of all the toxic-induced hepatic damages. Histological studies also supported the beneficial role of taurine against Cd-induced hepatic damages. Combining all, results suggest that taurine could protect hepatic tissues against Cd-induced oxidative stress probably through its antioxidant activity.
authors.affiliation: Department of Chemistry, Bose Institute, 93/1, Acharya Prafulla Chandra Road, Kolkata 700009, West Bengal, India.
authors.forename: Mahua
authors.initials: M
authors.lastname: Sinha
authors.forename: Prasenjit
authors.initials: P
authors.lastname: Manna
authors.forename: Parames C
authors.initials: PC
authors.lastname: Sil
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage* / Q000378:metabolism; D002104:Cadmium / Q000008:administration & dosage / Q000032:analysis / Q000633:toxicity*; D019256:Cadmium Chloride / Q000008:administration & dosage; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D053938:DNA Fragmentation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000032:analysis / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000737:chemistry / Q000201:enzymology / Q000473:pathology*; D008297:Male; D008668:Metallothionein / Q000032:analysis / Q000378:metabolism; D051379:Mice; D009336:Necrosis / Q000517:prevention & control; D009929:Organ Size; D018384:Oxidative Stress / Q000187:drug effects*; D010088:Oxidoreductases / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D011897:Random Allocation; D017382:Reactive Oxygen Species / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000032:analysis; D013654:Taurine / Q000008:administration & dosage* / Q000378:metabolism; D014131:Trace Elements / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D013438:Sulfhydryl Compounds; D014131:Trace Elements; D002104:Cadmium; D013654:Taurine; D003577:Cytochrome P-450 Enzyme System; D008668:Metallothionein; D010088:Oxidoreductases; D005982:Glutathione Transferase; D005978:Glutathione; D019256:Cadmium Chloride