Effect of the peroxisomal proliferator di(2-ethylhexyl)phthalate on component reactions of the rat hepatic microsomal fatty acid chain elongation system and on other hepatic lipogenic enzymes.
Effect of the peroxisomal proliferator di(2-ethylhexyl)phthalate on component reactions of the rat hepatic microsomal fatty acid chain elongation system and on other hepatic lipogenic enzymes.
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过氧化物酶体增殖剂邻苯二甲酸二（2-乙基己基）酯对大鼠肝微粒体脂肪酸链延长系统和其他肝脂肪生成酶的成分反应的影响。
DOI：
10.1016/0003-9861(86)90501-1
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发表时间：
1986
影响因子：
3.9
通讯作者：
Cinti,DL
中科院分区：
文献类型：
--
作者：
Prasad,MR;Cinti,DL
向大鼠喂食2%邻苯二甲酸二（2-乙基己基）酯（DEHP）使棕榈酰辅酶A的肝微粒体延长约2倍，而棕榈油酰辅酶A和γ-亚麻酰辅酶A的肝微粒体延长分别降至对照值的83%和63%。当测量延伸途径的组分反应时，观察到只有缩合酶的活性增加了两倍，而β-酮硬脂酰辅酶A还原酶、β-羟基棕榈酰辅酶A还原酶和反式-2-十六烯酰辅酶A还原酶的活性不受影响。此外，诱导棕榈酰辅酶A的缩合和延伸的时间过程是相似的。在体外加入DEHP对缩合或延伸没有影响。因此，这些结果表明，过氧化物酶体增殖物只诱导凝聚酶，这是延长序列的调节和限速步骤。DEHP处理还显著增强了胞浆葡萄糖-6-磷酸脱氢酶（2.2倍）和苹果酸酶（7.3倍）的NADPH生成活性。出乎意料的是，脂肪酸合成酶和柠檬酸裂解酶的活性不受影响。这些结果进行了讨论的事实，这些脂肪生成酶是协调诱导的饮食或激素。
The feeding of 2% di(2-ethylhexyl)phthalate (DEHP) to rats increased the hepatic microsomal elongation of palmitoyl-CoA by about twofold, while those of palmitoleoyl-CoA and γ-linolenoyl-CoA decreased to 83 and 63%, respectively, of the control values. When component reactions of the elongation pathway were measured, it was observed that only the activity of condensing enzyme was increased by twofold, while those of β-ketostearoyl-CoA reductase, β-hydroxypalmitoyl-CoA dehydrase, andtrans-2-hexadecenoyl-CoA reductases were not affected. Furthermore, the time course for induction of both condensation and elongation of palmitoyl-CoA was similar.In vitroaddition of DEHP had no effect on either condensation or elongation. Thus, these results indicate that the peroxisomal proliferator induces only the condensing enzyme which is the regulatory and rate-limiting step of elongation sequence. The DEHP treatment also markedly enhanced the cytosolic NADPH-generating activities of glucose-6-PO4dehydrogenase (2.2-fold) and malic enzyme (7.3-fold). Unexpectedly, the activities of fatty acid synthetase and citrate cleavage enzyme were unaffected. These results are discussed in light of the fact that these lipogenic enzymes are coordinatively induced by diet or hormones.