title: Attenuation of cadmium chloride induced cytotoxicity in murine hepatocytes by a protein isolated from the leaves of the herb Cajanus indicus L.
abstract: Cadmium has been recognized as a strong environmental pollutant. Exposure to this heavy metal occurs through the intake of foodstuffs, drinking water and also via the inhalation of air. Present study was conducted to evaluate the protective effect of a 43 kDa protein, isolated from the leaves of the herb Cajanus indicus, against cadmium-induced cytotoxicity in hepatocytes. For this study, cadmium chloride (CdCl(2)) has been used as the source of cadmium. Treatment of hepatocytes with 800 microM CdCl(2) for 3 h caused significant reduction in cell viability in association with the increased levels of glutamate pyruvate transaminase (GPT) and alkaline phosphatase (ALP) leakage. The activities of the antioxidant enzymes, superoxide dismutase, catalase (CAT), glutathione-S-transferase and glutathione reductase, and the levels of cellular metabolites, reduced glutathione (GSH) as well as total thiols have also been decreased under the same treatment. In addition, the toxin enhanced the levels of the lipid peroxidation end products and oxidized glutathione (GSSG). Incubation of hepatocytes with the protein at a dose of 0.1 mg/ml for 3 h prior to the toxin treatment (at a dose of 800 microM for 3 h) restored the activities of all the antioxidant enzymes, the levels of GSH, total thiols, cell viability and also attenuated the increased levels of GPT, ALP, lipid peroxidation and GSSG. In addition, the protein resisted CdCl(2) induced alterations of all the parameters when applied in combination with CdCl(2). Effects of a known antioxidant, vitamin E, and a non-relevant protein, bovine serum albumin against CdCl(2) induced cytotoxicity have also been included in the study. Combining all, we would like to say that the protein possessed protective activity against CdCl(2) induced cytotoxicity in mouse hepatocytes probably via its antioxidant property.
authors.affiliation: Department of Chemistry, Bose Institute, 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: D000410:Alanine Transaminase / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology*; D019256:Cadmium Chloride / Q000633:toxicity*; D036561:Cajanus / Q000737:chemistry; D002374:Catalase / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D019610:Cytoprotection; D004785:Environmental Pollutants / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D022781:Hepatocytes / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D008970:Molecular Weight; D018515:Plant Leaves; D010940:Plant Proteins / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology*; D012710:Serum Albumin, Bovine / Q000494:pharmacology; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D004785:Environmental Pollutants; D010940:Plant Proteins; D013438:Sulfhydryl Compounds; D014810:Vitamin E; D012710:Serum Albumin, Bovine; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase; D005978:Glutathione; D019256:Cadmium Chloride