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Human & Experimental Toxicology
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Effect of lipoic acid on the oxidoreductive status of red blood cells in rats subject to oxidative stress by chronic administration of adriamycin

K P Malarkodi

Department of Medical Biochemistry, Dr AL Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras (Taramani), Chennai 600 113, India; # 12/7, Desianathar Street, Poompuhar nagar, Edayarpalayam, Coimbatore 641 025, India, kurinjikp{at}rediffmail.com

R Sivaprasad

P Varalakshmi

Department of Medical Biochemistry, Dr AL Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras (Taramani), Chennai 600 113, India

One of the most intriguing phenomena observed during adriamycin (ADR) toxicity has been attributed to ADR-induced oxidative stress. The study was aimed to assess the protective effect of lipoic acid (LA) against ADR induced damage to erythrocytes. Male albino rats (Wistar strain) were subjected to ADR (1 mg/kg body weight/day i.v.) once a week for a period of 12 weeks. Haematological indices like haemoglobin levels (Hb) and haematocrit (Ht) were also lowered along with a marked increase in the activities of serum glutamate pyruvate transaminase (SGPT) and serum glutamate oxaloacetate transaminase (SGOT). These rats demonstrated enhanced erythrocyte membrane lipid peroxidation (LPO) and an onslaught in the antioxidant defence armoury, witnessed by lowered activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), vitamin A, vitamin C and vitamin E. Rats administered with ADR showed a marked decline in the activities of membrane-bound ATPases. Abnormal LPO and decreased deformability led to increased osmotic fragility of the red blood cells. Pretreatment with LA (35 mg/kg body weight/day i.p.) 24 hours prior to the administration of ADR once a week for a period of 12 weeks was effective in counteracting these biochemical disturbances, thereby minimizing the toxic side effects of ADR.

Key Words: adriamycin • antioxidants • DL-{alpha}lipoic acid • erythrocytes • lipid peroxidation

Human & Experimental Toxicology, Vol. 23, No. 3, 129-135 (2004)
DOI: 10.1191/0960327104ht428oa


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