N-3 FATTY ACID INTAKE AND LIPID PEROXIDATION PARADOX.

在这项研究中，组织过氧化脂质的形成后，摄入的n-3多不饱和脂肪酸，主要是二十二碳六烯酸，脂质过氧化物清除剂和脂肪酸组成的总脂质，中性脂质和磷脂在一些组织中进行了研究。结果，响应于增加的膳食DHA水平，在诸如肝、肾、脑和睾丸的组织中产生的脂质过氧化物水平不像根据组织总脂质的脂肪酸组成计算的过氧化指数所预期的那样高。同时未观察到组织损伤。推测在过氧化指数下抑制的原因如下。1)水溶性抗氧化剂如抗坏血酸和谷胱甘肽的水平增加，导致生育酚从生育酚氧基自由基的还原再生的刺激。2)n-3多不饱和脂肪酸，尤其是DHA，在组织中的整合因组织而异，并且DHA低的组织形成较少的脂质过氧化物。3)DHA优先用于磷脂酰乙醇胺（PE）的合成，PE的抗氧化稳定性被认为是通过与VE共存而增强的。4)结合DHA的磷脂的构象变化可能导致稳定的形式，因此，它可能增加对氧化产物的稳定性。5)过氧化物酶体β-氧化刺激易受氧化的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.