Amelioration of cadmium-induced cardiac impairment by taurine.
The present study has been designed to investigate the protective role of taurine (2-aminoethanesulfonic acid), a sulfur containing conditionally essential amino acid, against cadmium-induced cardiac dysfunction in mice. Cadmium chloride (CdCl(2)) was used as the source of cadmium and it was administered orally at a dose of 4mg/kg body weight for 6 days. Cadmium exposure caused significant accumulation of the cadmium and iron in mice hearts tissue. Levels of serum specific markers related to cardiac impairments, e.g. total cholesterol, HDL cholesterol and triglyceride were altered due to cadmium toxicity. Reduction in the activities of antioxidant enzymes, namely, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PD) have been observed in cadmium exposed mice. Cadmium intoxication also decreased the cardiac glutathione (GSH) and total thiols contents and increased the levels of oxidized glutathione (GSSG), lipid peroxidation end products, protein carbonyl content and the extent of DNA fragmentation. Oral administration of taurine at a dose of 100mg/kg body weight for 5 days, however, prevented all the toxin-induced oxidative impairments mentioned above. "Ferric Reducing/Antioxidant Power (FRAP) assay" showed that taurine could protect the cardiac tissue by preventing cadmium-induced reduction of the intracellular antioxidant power. Histological examination of cardiac segments also supported the beneficial role of taurine against cadmium-induced damages in the murine hearts. Effect of a well established antioxidant, vitamin C has been included in the study as a positive control. Combining all, results suggest that taurine attenuates cadmium-induced impairment in mice hearts.
Manna
Prasenjit
P
Department of Chemistry, Bose Institute, Kolkata 700009, West Bengal, India.
Sinha
Mahua
M
Sil
Parames C
PC
D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D019256:Cadmium Chloride / Q000633:toxicity*; D018890:Chemoprevention; D053938:DNA Fragmentation / Q000187:drug effects; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004785:Environmental Pollutants / Q000633:toxicity*; D004798:Enzymes / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D051379:Mice; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress; D013654:Taurine / Q000008:administration & dosage*
D000975:Antioxidants; D015415:Biomarkers; D004785:Environmental Pollutants; D004798:Enzymes; D013654:Taurine; D019256:Cadmium Chloride