title: Cadmium-induced lipid peroxidation and the antioxidant system in rat erythrocytes: the role of antioxidants.
abstract: Cadmium (Cd)-induced oxidative damage in erythrocytes causes loss of membrane function by enhancing lipid peroxidation (LPO) and altering the erythrocyte antioxidant system. Vitamin E and/or selenium (Se) was administered to rats, prior to Cd intoxication, in order to prepare the animals to withstand oxidative assault. The treatment with Cd increased LPO in erythrocytes while animals pretreated with vitamin E and/or Se prior to Cd treatment showed decreased LPO as compared with animals given Cd alone. The erythrocyte SOD and CAT activities decreased significantly with Cd treatment. The pretreatment with vitamin E and/or Se prior to Cd administration partially reversed such changes. The erythrocytes showed a marked depletion in glutathione (GSH) content with Cd treatment. The antioxidant treatments before Cd administration helped to maintain the erythrocyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treatments with vitamin E and Se were applied. The GSH-R activity was not observed to decrease in animals treated with antioxidant prior to Cd intoxication, which may mean that the replenishment of erythrocyte GSH content is via GSH-R. The glutathione-S-transferase (GST) activity increased significantly with Cd intoxication; however, treatment with antioxidants prior to Cd treatment decreased erythrocyte GST activity. The results show that Cd-induced LPO decreased the antioxidant capability of the erythrocytes, causing erythrocyte membrane damage.
authors.affiliation: Centre for Reproductive Biology and Molecular Endocrinology, Indian Institute of Science, Bangalore, India.
authors.forename: S
authors.initials: S
authors.lastname: Sarkar
authors.forename: P
authors.initials: P
authors.lastname: Yadav
authors.forename: D
authors.initials: D
authors.lastname: Bhatnagar
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D019256:Cadmium Chloride / Q000494:pharmacology*; D002374:Catalase / Q000097:blood; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005978:Glutathione / Q000097:blood*; D005980:Glutathione Reductase / Q000097:blood; D005982:Glutathione Transferase / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D051381:Rats; D018038:Sodium Selenite / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D018038:Sodium Selenite; D019256:Cadmium Chloride