Docosahexaenoic acid intake potentiates antioxidative potential in vivo

在之前的研究中，我们发现摄入二十二碳六烯酸（DHA）增加了大鼠肝脏和肾脏对脂质过氧化的敏感性，但并没有使脂质过氧化形成达到组织总脂质的相对过氧化物指数（p指数）所期望的水平。结果表明，dha刺激的组织脂质过氧化形成存在一定的抑制机制，如观察到组织抗坏血酸（AsA）和谷胱甘肽（GSH）水平升高。此外，我们提出二十二碳六烯酸（DHA）掺入磷脂酰乙醇胺（PE）可能增强体内对脂质过氧化的抵抗。因此，在本研究中，我们首先关注AsA和/或GSH在抑制机制中的作用，然后关注PE的跨双层分布与DHA与PE结合的氧化稳定性之间的关系。我们研究了膳食中不同水平的AsA和蛋氨酸对需要维生素c的ODS大鼠肝脏过氧化脂质和抗氧化剂水平的影响，其中蛋氨酸是合成谷胱甘肽所必需的。我们发现生理水平的AsA和蛋氨酸可以抑制dha刺激的脂质过氧化形成和维生素E的消耗，但超过生理水平的AsA和蛋氨酸并不能进一步抑制维生素E的形成和消耗。此外，当大鼠摄入低水平蛋氨酸时，肝脏脂质过氧化形成和谷胱甘肽- s转移酶活性增加。这些结果表明AsA和GSH增强了有限的抗氧化能力。因此，其他因素，如谷胱甘肽- s转移酶对脂质过氧化物的解毒作用，可能与抑制机制有关。此外，为了调节从DHA喂养的大鼠肝脏中获得的PE （PE-DHA）的跨双层分布，我们使用了具有两种酰基链片段的磷脂酰胆碱（PC）：双棕榈酰（PC 16:0）和二油基（PC 18:1）。PC18: 1脂质体中PE-DHA在脂质体外层的比例显著高于PC16: 0脂质体。这种趋势在使用孔径较小的聚碳酸酯过滤器挤出的脂质体中更为明显。此外，使用孔径较小的过滤器制备的脂质体的外层PE-DHA可以保护DHA本身免受2,2 ' -偶氮（2-氨基丙烷）二盐酸盐介导的脂质过氧化作用。少

In previous studies, we showed that docosahexaenoic acid (DHA) ingestion enhance the susceptibility of rat liver and kidney to lipid peroxidation but did not increase lipid peroxide formation to the level expected from the relative peroxidizability index (P-index) of the total tissue lipids. The results suggested the existence of some suppressive mechanisms against DHA-stimulated tissue lipid peroxide formation, as observed increased tissue ascorbic acid (AsA) and glutathione (GSH) levels. Furthermore, we have proposed that incorporation of docosahexaenoic acid (DHA) into phosphatidylethanolamine (PE) might enhance resistance to lipid peroxidation in vivo.In this study, therefore, we focused initially on the roles of AsA and/or GSH for the suppressive mechanisms and secondly on the relationship between the transbilayer distribution of PE and oxidative stability of DHA combined with PE.We examined the influences of different levels of dietary AsA and methionine, the latter of which is r … More equired for GSH-synthesis, on the liver lipid peroxide and antioxidant levels in vitamin C-requiring ODS rats. We found that physiological levels of AsA and methionine were required for suppressing DHA-stimulated lipid peroxide formation and consumption of vitamin E, but the dietary AsA and methionine over physiological levels did not suppress further the formation and consumption. In addition, when rats ingested a low level of methionine, liver lipid peroxide formation and glutathione-S-transferase activity were increased. These results suggested a limited antioxidant ability potentiated by AsA and GSH. Therefore, other factor such as detoxification of lipid peroxides by glutathione-S-transferase, may be related to the suppressive mechanisms.In addition, to modulate the transbilayer distribution of PE (PE-DHA) obtained from the liver of rats fed DHA, we used phosphatidylcholine (PC) with two types of acyl chain moiety: dipalmitoyl (PC 16 : 0) and dioleoyl (PC 18 : 1). The proportion of PE-DHA in the liposomal external layer was significantly higher in liposomes containing PC18 : 1 than in those containing PC16 : 0. This tendency was more pronounced in liposomes extruded using a polycarbonate filter with smaller pore sizes. Additionally, PE-DHA in the external layer of liposomes prepared using a filter with smaller pore sizes could protect DHA itself from 2, 2' -azobis (2-amino-propane) dihydrochloride -mediated lipid peroxidation. Less