µ-Lipoic acid (ALA) is a naturally occuring cofactor that serves as an acyl carrier in oxidative decarboxylation of _-keto acids in carbohydrate metabolism. Current findings suggest that _-lipoic acid and its reduced form, dihydrolipoic acid (DHLA) may act as antioxidants and are able to quench free radicals in vitro and in vivo. However, the mechanism underlying the process is still unknown. In this study, atherosclerotic lesions were induced in six groups of adult male NZW rabbits labelled as group K, A, B, C, D, E (n=6) by giving 100g/head/day of 2% cholesterolrich diet for ten weeks. While group K acted as a control, the rest were supplemented with ALA orally (1.4, 2.8, 4.2, 8.0 and 10mg/kg, respectively). In week ten, venous blood samples drawn from ear lobes were analysed for complete lipid profile and peroxidation index. The results showed a significant reduction of total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) levels in most of the treated groups as compared to the control whereas apo-A levels showed a significant increase in group C and D. However, microsomal lipid peroxidation index, malondialdehyde (MDA) was found to be not significantly different. These findings suggest that µ-lipoic acid may act as a lipid lowering agent in dose dependent manner in premature stage of atherosclerosis but was unable to inhibit lipid peroxidation processes in matured stage of atherosclerosis in rabbits fed a high cholesterol diet.