Journal of 1. Trace Elements Med. BioI. Vol. II. pp. 8-13 (J 997) Trace Elements In Medicine and Biology © 1997 by Gustav Fischer Verlag Cadmium-Induced Lipid Peroxidation and the Antioxidant System in Rat Erythrocytes: the Role of Antioxidants S. SARKAR, P. YADAV* and D. BHATNAGAR**·I Centre for Reproductive Biology and Molecular Endocrinology, *Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India. **School of Biochemistry, D.A. University, Khandwa Road, Indore 45200 I, India. (Received April/September 1996) Summary 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 ad- ministration 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 erythro- cyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treat- ments 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; how- ever, 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. Keywords: Lipid peroxidation, superoxide dismutase, catalase, glutathione, cadmium, selenium. Introduction reactions. The lipid peroxides and lipid radicals along with other toxic species such as OH and O 2 radicals Cadmium exposure is known to produce damaging cause peroxidation of membrane lipids with the genera- effects in humans and in various laboratory animals (I). tion of aldehydes such as malonyldialdehyde and hy- The action of Cd involves oxidative damage to cell mem- droxyalkenals (5,6). The unsaturated fatty acids present branes manifested through peroxidation of membrane li- in the membranes (phospholipids, glycolipids and ster- pids and by altering the antioxidant capability of the cells ols) and the trans-membrane proteins containing oxidiza- (2-4). The effect of Cd toxicity was observed in erythro- ble amino acids are susceptible to free radical damage cytes as they are more vulnerable to oxidative damage (7). The peroxidation of membrane lipids is mainly coun- due to the high oxygen tension, presence of poly-unsatu- teracted by vitamin E present in the cellular lipid environ- rated fatty acids and iron, a potent catalyst for free radical ment which maintains the membrane integrity (8). The ITo whom correspondence should be addressed. role of selenium as an antioxidant has been proven and it