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Updated: Jun 27, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
High-cholesterol diet increases xanthine oxidase and decreases nitric oxide synthase activities in erythrocytes from
Erdinç Devrim1, Imge B Ergüder, Hanefi Ozbek
1Department of Biochemistry, Ankara University Faculty of Medicine, 06100 Ankara, Turkey. erdincdevrim@yahoo.com
Abstract:
The aim of this study was to investigate the effects of a high-cholesterol diet on oxidant/antioxidant status and nitric oxide synthase (NOS) activity in erythrocytes from rats. Sixteen Sprague-Dawley-type albino male rats were used in the study. The rats were randomly divided into 2 groups: the control group (group 1) was fed a standard rat diet, and the treated group (group 2) was fed a high-cholesterol diet (4% cholesterol, 1% cholic acid, and 0.5% thiouracil) in addition to standard pellet rat diet for 3 months. At the end of the study period, blood samples were obtained from the rats under ether anesthesia. Oxidant (malondialdehyde level, sensitivity to oxidation value, and xanthine oxidase [XO] activity) and antioxidant parameters (antioxidant potential value, superoxide dismutase, catalase, and glutathione peroxidase activities) were studied in erythrocyte preparations. Activities of erythrocyte NOS and arginase enzymes and serum total cholesterol levels were also measured. We observed that serum total cholesterol levels, erythrocyte XO activities, and sensitivity to oxidation values significantly increased in group 2 (cholesterol fed) compared with the control group (group 1). Erythrocyte NOS activities were also found to decrease in group 2. In conclusion, our results suggest that cholesterol feeding causes an increase in XO activity and a decrease in NOS activity in the erythrocytes from rats. The increase in XO activity may render the erythrocyte membranes sensitive to oxidant stress, and the decrease in NOS activity in the erythrocytes may increase cardiovascular disease risk via reduced endothelial relaxation.
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