肝脏内质网中存在NADH时脂肪酸延伸率较低。牛血清白蛋白在β-酮还原酶水平上过度抑制。
Low fatty acid elongation rate in the presence of NADH in the liver endoplasmic reticulum. Overinhibition by BSA at the beta-ketoreductase level.
作者信息
Demirkapi N, Ghesquier D
机构信息
Institut National de la Santé et de la Recherche Médicale, U 56, Hôpital de Bicêtre, Le Kremlin-Bicêtre, France.
出版信息
Biochim Biophys Acta. 1990 Sep 18;1046(2):229-32. doi: 10.1016/0005-2760(90)90194-3.
The rate of NADH-dependent palmitoyl-CoA elongation was only 41% of that of NADH-dependent elongation in microsomes from rats fed a fat-free diet, in the absence of BSA. This value was markedly lowered to 5%, when the assay was performed in the presence of BSA. The determination of the intermediate products showed that 93% of the total products accumulated as beta-ketostearate in the presence of BSA and NADH, whereas the accumulated beta-ketostearate was only 25% of the total products in the presence of BSA and NADPH. BSA was shown to be responsible for the low rate of NADH-dependent elongation by inhibiting the beta-ketoreductase in the presence of NADH and, thereby, inducing beta-ketostearate accumulation. These results indicate that NADH is probably not the physiological electron donor to the elongation pathway.
在无牛血清白蛋白（BSA）存在的情况下，喂食无脂饮食的大鼠微粒体中，NADH依赖的棕榈酰辅酶A延长速率仅为NADH依赖延长速率的41%。当在有BSA存在的情况下进行测定时，该值显著降低至5%。中间产物的测定表明，在有BSA和NADH存在时，93%的总产物以β-酮硬脂酸的形式积累，而在有BSA和NADPH存在时，积累的β-酮硬脂酸仅占总产物的25%。结果表明，BSA通过在NADH存在时抑制β-酮还原酶，从而导致β-酮硬脂酸积累，进而导致NADH依赖的延长速率降低。这些结果表明，NADH可能不是延长途径的生理电子供体。
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