首页> 外文期刊>Prostaglandins, Leukotrienes, and Essential Fatty Acids >Arachidonic and docosahexaenoic acids differentially affect the expression of fatty acyl-CoA oxidase, protein kinase C and lipid peroxidation in HepG2 cells.
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Arachidonic and docosahexaenoic acids differentially affect the expression of fatty acyl-CoA oxidase, protein kinase C and lipid peroxidation in HepG2 cells.

机译:花生四烯酸和二十二碳六烯酸差异影响HepG2细胞中脂肪酰基辅酶A氧化酶,蛋白激酶C和脂质过氧化的表达。

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摘要

Arachidonic (AA) and docosahexaenoic (DHA) acids (5-20 microM), when supplemented to human hepatoma HepG2 cells, which are depleted in these long-chain polyunsaturated fatty acids in conventional culture conditions, enhance the expression of acyl-CoA oxidase (ACOX), the first enzyme in the peroxisomal beta-oxidation cycle. DHA is effective at lower concentrations (at 5 microM) and to a greater extent (about 60% increment) than AA (about 40%) at 20 microM. Protein kinase C (PKC) appears to be involved in the activity of AA on ACOX, but not in that of DHA, since only the effect of AA is prevented by the PKC inhibitor Staurosporine, and since a remarkable elevation of the PKC activator diacylglycerol occurs only after AA supplementation. AA also induces elevation of lipoperoxides, favoured by the relative vitamin E deficiency occurring in cultured cells, and this effect, which is prevented by supplementation of the vitamin, may contribute to PKC activation.
机译:花生四烯酸(AA)和二十二碳六烯酸(DHA)酸(5-20​​ microM)在补充人类肝癌HepG2细胞后,在常规培养条件下会耗尽这些长链多不饱和脂肪酸,从而增强酰基辅酶A氧化酶的表达(过氧化物酶体β-氧化循环中的第一种酶。与20 microM的AA(约40%)相比,DHA在较低的浓度(5 microM)和更大的程度上(约60%增量)有效。蛋白激酶C(PKC)似乎与AA对ACOX的活性有关,但与DHA无关,因为PKC抑制剂Staurosporine仅阻止了AA的作用,并且由于PKC活化剂二酰基甘油的显着升高只有在补充AA后。 AA也可引起脂过氧化物的升高,这是由于培养细胞中出现的相对维生素E缺乏所致,这种作用(可通过补充维生素来防止)可能有助于PKC活化。

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