N-3 FATTY ACID INTAKE AND LIPID PEROXIDATION PARADOX.

在本研究中，研究了摄入n-3多不饱和脂肪酸(主要是二十二碳六烯酸)后组织脂质过氧化的形成与脂质过氧化清除剂以及某些组织中总脂、中性脂和磷脂的脂肪酸组成的关系。因此，从组织总脂的脂肪酸组成计算的过氧化指数来看，肝脏、肾脏、脑和睾丸等组织产生的过氧化脂质水平并不像预期的那样高。同时也没有观察到组织损伤。在过氧化性指数下抑制的原因推定如下。1)维生素C、谷胱甘肽等水溶性抗氧化剂含量增加，促进生育酚从生育氧自由基中还原再生。2)n-3多不饱和脂肪酸，尤其是DHA在不同组织中的转运情况不同，DHA含量低的组织形成的过氧化脂质较少。3)DHA优先用于磷脂酰乙醇胺(PE)的合成，与VE共存可增强PE的抗氧化稳定性。4)结合DHA的磷脂的构象变化可能导致DHA的稳定形式，从而增强其抗氧化稳定性。5)过氧化体β氧化促进了易氧化的DHA的代谢降解。

In this study, tissue lipid peroxide formation after ingestion of n-3 polyunsaturated fatty acids, primarily docosahexaenoic acid, was investigated in relation to lipid peroxide scavengers and fatty acid compositions of total lipids, neutral lipids and phosholipids in some tissues. As a result, the lipid peroxide levels produced in tissues such as liver, kidney, brain and testis in response to increasing levels of dietary DHA were not as high as expected from the peroxidizability indexes which were calculated from the fatty acid compositions of tissue total lipids. No tissue injuries were also observed concurrently. The reasons to suppress under the peroxidizability index were presumed as follows. 1) The levels of water-soluble antioxidants such as ascorbic acid and glutathione were increased, leading to stimulation of reductive regeneration of tocopherols from tocopheroxyl radicals. 2) Incorportation of n-3 polyunsaturated fatty acids, especially DHA, into tissues differed from tissue to tissue, and the tissue low in DHA formed less lipid peroxides. 3) DHA was preferentially utilized for phosphatidylethanolamine (PE) synthesis and the antioxidative stability of PE was thought to be potentiated by coexistence with VE. 4) Conformational changes of phospholipids which bind DHA may lead to a stabilized form, and thus, it may augment stability against oxidation resultantly. 5) Peroxisomal β-oxidation stimulates metabolic degradation of DHA vulnerable to oxidation.