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Experimental Atherosclerosis and Oxygen Free Radicals

Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada

Jawahar Kalra

Department of Pathology, College of Medicine, University of Saskatchewan and University Hospital, Saskatoon, Saskatchewan, Canada

Oxygen free radicals are known to produce cellular injury by peroxidation of phospholipids in the cell membrane. These free radicals might damage the endothelial cell and thus set the stage for atherosclerosis. The authors studied the effect of high-cholesterol diets on the genesis of atherosclerosis and lipid peroxidation products, malondialdehyde (MDA) in rabbits. The animals were divided into four groups each comprising 5 rabbits, on the basis of their diets. Group I, control diet; group II, cholesterol; group III, coconut oil; group IV, a mixture of cholesterol, coconut oil, and cholic acid. Rabbits were sacrificed five months after being on the respective diets. Blood samples were obtained for the measurements of total cholesterol, high density lipoprotein cholesterol (HDL- C), low density lipoprotein cholesterol (LDL-C), very low density lipoprotein cholesterol (VLDL-C), triglycerides, and MDA at the end of the protocol. The aortas were removed from different animals for the identification of athero sclerotic plaques. Plaques were detected in all the animals in group II and group IV. The serum total cholesterol, LDL-C, and VLDL-C were significantly higher in animals of group II and IV than in those of group I. The values for serum total cholesterol, HDL-C, LDL-C, and VLDL-C in group III were not signifi cantly different from those in group I. The blood MDA and serum triglycerides were also higher in animals of group II and IV than in those of group I. There were, however, no significant differences in these parameters in group III as compared with those in group I. This study showed that there was an increase in the lipid peroxidation product (MDA) in all those rabbits that had atheroscler otic changes in the aorta. This increase might be due to an increase in oxygen free radicals, which may be involved in the genesis and maintenance of choles terol-induced atherosclerosis.

Angiology, Vol. 40, No. 9, 835-843 (1989)
DOI: 10.1177/000331978904000911


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