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维生素E对大鼠血小板中花生四烯酸代谢的体内外作用。

In vitro and in vivo effects of vitamin E on arachidonic acid metabolism in rat platelets.

作者信息

Hwang D H, Donovan J

出版信息

J Nutr. 1982 Jun;112(6):1233-7. doi: 10.1093/jn/112.6.1233.

Abstract

Preincubating platelet-rich plasma (PRP) of vitamin E-deficient rats with RRR-alpha-tocopherol prior to the aggregation induced by collagen suspension resulted in inhibition of the formation of endoperoxide metabolites derived from endogenous arachidonic acid (AA). This inhibition was not dose dependent at concentrations above the plasma level of RRR-alpha-tocopherol of vitamin E-supplemented rats. Preincubating the vitamin E-deficient PRP with RRR-alpha-tocopherol did not affect the formation of 12-hydroxyeicosatetraenoic acid, the platelet lipoxygenase product. Concentrations of endoperoxide metabolites in diluted whole blood challenged with collagen suspension were significantly greater in the vitamin E-deficient group than the supplemented group. The level of AA in platelet or plasma phospholipids was not different between the two groups. However, blood platelet counts in the deficient group were significantly greater than those of the supplemented group. Concentrations of endoperoxide metabolites in PRP samples in which platelet concentrations were equalized were still greater in vitamin E-deficient group; however, the difference was not statistically significant. There was also no difference in the degree of maximal platelet aggregation between the two groups. These results indicated that vitamin E deficiency can slightly stimulate the formation of cyclooxygenase products derived from endogenous AA, but it did not affect the formation of lipoxygenase product in rat platelets.

摘要

在用胶原蛋白悬液诱导聚集之前,将维生素E缺乏大鼠的富含血小板血浆(PRP)与RRR-α-生育酚预孵育,可抑制内源性花生四烯酸(AA)衍生的内过氧化物代谢产物的形成。在高于补充维生素E大鼠的RRR-α-生育酚血浆水平的浓度下,这种抑制作用不依赖剂量。用RRR-α-生育酚预孵育维生素E缺乏的PRP不影响血小板脂氧合酶产物12-羟基二十碳四烯酸的形成。用胶原蛋白悬液刺激的稀释全血中内过氧化物代谢产物的浓度在维生素E缺乏组中显著高于补充组。两组血小板或血浆磷脂中的AA水平没有差异。然而,缺乏组的血小板计数显著高于补充组。在血小板浓度相等的PRP样品中,维生素E缺乏组的内过氧化物代谢产物浓度仍然较高;然而,差异无统计学意义。两组之间最大血小板聚集程度也没有差异。这些结果表明,维生素E缺乏可轻微刺激大鼠血小板中源自内源性AA的环氧化酶产物的形成,但不影响脂氧合酶产物的形成。

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