Journal Name:
Lipids
Article Title:
Plasma and lipoprotein lipid peroxidation in humans on sunflower & rapeseed oil diets
Date Written:
1995
Volume:
30
Number:
6
Page:
485
Author(s):
Turpeinen, A.; Alfthan, G.; Valsta, L.; Hietanen, E.; Salonen, J.; Schunk, H.; Nyyss�nen, K.; Mutanen, M.
Article:
Increased lipid peroxidation is believed to be involved in CHD, diabetes mellitus, cancer, inflammatory diseases and possibly toxicity. Oxidized LDL products have been found in atherosclerotic lesions of animals and humans. Specific receptors that recognize oxidized LDL-C, but not unmodified LDL-C, have been identified and have been shown not to be down regulated through normal mechanisms, leading to the production of lipid-laden foam cells. Antioxidants such as Vitamin E, which is present in CO, can protect PUFAs in LDL lipids from oxidation. In addition, OA is much less susceptible (approximately 10 times) to oxidation than LA, suggesting that oils with higher levels of OA such as CO would be less likely to stimulate LDL-C oxidation than oils high in LA such as sunflower. The generation of conjugated dienes in LDL in vitro has been found to be significantly depressed in humans consuming a high OA diet in comparison with one high in LA.
This study was conducted in two parts and assessed the effects of diets containing either CO or sunflower oil on lipid peroxidation. In the first study, 59 subjects (18 to 60 years old) were fed either CO or a sunflower oil-based (SO) diet in a cross-over design for 3.5 weeks. During the first 14 days, subjects were fed a high SFA diet, after which 30 subjects consumed a high SO diet for 24 days followed by the CO diet for 24 days. The remaining 29 subjects consumed the diets in the reverse order. Total fat contributed about 38% of energy and was comprised of 13% SFA, 10% MUFA (SO diet) or 16% MUFA (CO diet) and 13% PUFA (SO diet) or 8% PUFA (CO diet). Lipid peroxidation products in plasma were estimated by measuring conjugated dienes (primary oxidation products) and malondialdehyde (MDA - produced through the breakdown of FA with 3 or more double bonds). No significant differences in plasma MDA or conjugated diene concentrations were found following either diet, although less MDA was present in the CO dietary group when measured by a spectrophotometric method. Plasma alpha-tocopherol significantly increased from 4.8 to 6.4 mg/L following the CO diet and no changes were noted after the SO diet.
In the second study, plasma thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides and the susceptibility of VLDL + LDL to in vitro oxidation were measured in 6 and 7 subjects, respectively, fed CO and sunflower oil diets for 6 weeks. Approximately 50 g of test oil/day were added to the normal diets of the subjects. The percentage of energy obtained from MUFA and PUFA in the CO and SO diet were 18.3 and 9.0, and 12.1 and 15.6, respectively, and SFA content of both diets was approximately 12%. A small, but significant, decrease in lipid hydroperoxides and TBARS was observed in the LDL fraction following the SO diet. In vitro oxidation produced opposite results, showing increased oxidation of LDL, measured as the production of conjugated dienes, following the SO diet. This finding is in agreement with a number of studies that have assessed lipid oxidation after either high MUFA or PUFA diets. Higher levels of conjugated dienes following the SO diet are in accordance with the theory that diene conjugation in humans is associated mainly with the metabolism of LA.
The results suggest that moderate changes in the fatty acid composition of a Western style diet may be adequate to affect lipoprotein susceptibility to oxidation in vitro. However, the authors conclude that results from lipid peroxidation studies must be viewed with caution as there appears to be disparity with some measurements of in vivo lipid peroxidation. They suggest that further research is required to establish whether any relationship exists between enhanced chemical oxidation in vitro and disease processes associated with in vivo lipid peroxidation., , , , ,
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