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The effect of a moderately oxidized soybean oil on lipid peroxidation in rat low-density lipoproteins at low and high dietary vitamin E levels

Eder, K., Kirchgessner, M.
Journal of animal physiology and animal nutrition 1997 v.78 no.1-5 pp. 230-243
adverse effects, atherosclerosis, coconut oil, dietary fat, fatty acid composition, fatty acids, feed intake, ingestion, lipid peroxidation, low density lipoprotein, macrophages, nutritional adequacy, oxidation, peroxide value, rats, soybean oil, thiobarbituric acid-reactive substances, vitamin E
SUMMARY: The present study was performed to investigate whether a moderately oxidized dietary oil influences lipid peroxidation processes in low-density lipoproteins (LDL) which have been demonstrated to play an important role in the development of atherosclerosis. Therefore, growing male rats were fed diets containing either a mixture of coconut oil and soybean oil (19:1, w: w), fresh soybean oil, or heated soybean oil as sources of dietary fats over a period of 40 days. Lipids of those diets were characterized by a peroxide value of 5.1, 9.5, and 74 mEq O₂/kg, respectively, on average over the whole feeding period. Additionally, according to a bifactorial design, the vitamin E supply of the animals was varied (11 versus 511 mg α-tocopherol equivalents per kg of diet). Feeding the diets containing the oxidized oils did not affect feed intake and growth, and, with the exception of reduced triglyceride concentrations, did not cause considerable alterations of plasma and lipoproteins lipids. The resistance of LDL against copper-induced lipid peroxiation was predominately influenced by dietary fatty acids and dietary vitamin E levels whereas the oxidation status of the oil had only a small effect. Feeding the coconut oil diet markedly increased lag times compared to feeding the soybean oil diets, and feeding the high-vitamin E diets markedly increased lag times compared to feeding the low-vitamin E diets. At the low dietary vitamin E level, feeding the oxidized soybean oil slightly reduced the lag time before onset of lipid peroxidation compared with rats fed fresh soybean oil. This effect might be due to reduced tocopherol concentrations in the LDL of those rats; the fatty acid composition of LDL lipids was not different between feeding fresh and oxidized soybean oil. At the high dietary vitamin E level, parameters measured to assess the LDL oxidation were completely indifferent between rats fed fresh and those fed oxidized soybean oil. Hence, the study suggests that a moderately oxidized oil at a nutritionally adequate vitamin E supply has no adverse effects on the resistance of LDL to peroxidation. However, the LDL of rats fed oxidized soybean oil had markedly higher concentrations of thiobarbituric acid-reactive substances (TBARS) than the LDL of rats fed coconut oil or fresh soybean oil. Vitamin E supplementation reduced the TBARS concentrations in rats fed the oxidized oil; nevertheless, the TBARS concentrations remained higher than in rats fed fresh soybean oil. Probably, the increased concentrations of TBARS in LDL are due to the incorporation of dietary lipid peroxidation products into endogenous lipoproteins. Increased concentrations of peroxidation products in LDL after ingestion of oxidized fats could be of clinical relevance because oxidatively modified LDL are taken up by macrophages leading to the formation of fatty streaks.