Casein and soy protein isolate in experimental atherosclerosis: influence on hyperlipidemia and lipoprotein oxidation.

BACKGROUND/AIMS: Nutrients able to modify the susceptibility of lipoproteins to oxidation and/or reduce the cholesterol levels of blood plasma are important for prevention and/or treatment of atherosclerosis. The influence of animal and vegetable proteins on hypercholesterolemia and atherogenesis has been studied, concerning the mechanisms able to modify the digestion, absorption and bioavailability of lipids. In this study, the influence of casein and soy protein isolate on lipoprotein oxidation and atherosclerosis progression was investigated in cholesterol-fed rabbits. METHODS: During 2 months, 20 New Zealand rabbits were fed with diets containing 1% cholesterol and 27% casein or 27% soy protein isolate. Blood samples were collected at baseline, 15, 30, 45 and 60 days of feeding. RESULTS: Casein feeding contributed to increasing cholesterol and triglyceride concentrations, lipoprotein oxidation and the area of aorta atherosclerotic lesions. In contrast, the soy protein isolate reduced, when compared to casein, the concentrations of cholesterol and lipid peroxides of beta-VLDL and LDL fractions during the experimental time course, as well as the area of atherosclerotic lesions at the end of the study. CONCLUSION: Soy protein isolate, in comparison with casein, promoted a decrease of lipid peroxides, cholesterol and triglyceride content of atherogenic lipoproteins (beta-VLDL and LDL), which had beneficial effects over atherosclerosis progression in cholesterol-fed rabbits.

Soy protein isolate reduces the oxidizability of LDL and the generation of oxidized LDL autoantibodies in rabbits with diet-induced atherosclerosis.

The incidence of atherosclerosis can be modified by diet, and plant-derived proteins have a beneficial effect, but the underlying mechanisms remain unclear. It has been suggested that oxidized LDL (oxLDL) and autoantibodies against oxLDL are important in the development of atherosclerosis. We analyzed these factors in rabbits fed a nonpurified diet supplemented with high cholesterol (10.0 g/kg) containing either 270.0 g/kg casein (CAS, n = 10) or 270.0 g/kg soy protein isolate (SPI, n = 10) for 2 mo. Plasma and purified serum LDL from rabbits were analyzed at d 0, 15, 30, 45 and 60 of treatment, and the size of atherosclerotic lesions was evaluated at d 60 of treatment. CAS-fed rabbits had significantly higher plasma cholesterol at d 15-45 and LDL cholesterol levels at d 15 and 30. Levels of trilinolein and phosphatidylcholine hydroperoxides were higher in the LDL fraction of rabbits fed CAS than in those fed SPI. Also, CAS-fed rabbits had higher levels of highly oxidized LDL [monoclonal antibody (mAb) 24-reactive oxLDL] in plasma at d 60, whereas SPI-fed rabbits had higher levels of minimally oxidized LDL (mAb 28-reactive oxLDL) at d 45. These results were consistent with the earlier formation of anti-oxLDL antibodies and the presence of a larger area of atherosclerotic lesion in rabbits fed the CAS diet. These data indicate the importance of both the type of dietary protein used in the induction of atherosclerosis and the relevance of immunologic mechanisms in addition to biochemical and physiologic factors in the pathogenesis of atherosclerosis.

Oxidized lipoproteins in blood plasma: possible marker of atherosclerosis progression.

Oxidized lipoproteins and antioxidants were detected during the course of hypercholesterolemia development in cholesterol-fed rabbits. Lipid peroxides in blood plasma and very-low-, low-, and high-density lipoproteins (beta-VLDL, LDL, and HDL) were increased during the course of hypercholesterolemia. The content of phospholipid peroxides increased in beta-VLDL and LDL in parallel to that of cholesterol, whereas the amount of alpha-tocopherol was decreased either in lipoproteins or blood plasma. Ascorbate and urate concentrations were also decreased. Lipid peroxides were positively correlated with volume and area of atherosclerotic lesions, suggesting a relation between the concentrations of lipid peroxides in blood plasma and the progression of atheromatous lesions.