VITAMIN E PROTECTION OF MEMBRANE LIPIDS DURING ELECTRON TRANSPORT FUNCTIONS *
VITAMIN E PROTECTION OF MEMBRANE LIPIDS DURING ELECTRON TRANSPORT FUNCTIONS *
复制标题
维生素 E 在电子传输功能期间对膜脂的保护 *
DOI：
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复制
发表时间：
1972
影响因子：
5.2
通讯作者：
William H. Stipe
中科院分区：
文献类型：
--
作者：
P. McCay;P. Pfeifer;William H. Stipe
Beloff-Chain and colleagues,' while investigating electron transport associated with TPNH oxidation in order to determine whether the oxygen uptake was accompanied by phosphorylation of ADP, found that such phosphorylation did not take place, but they did find a stoichiometric excess in the amount of oxygen consumed. In examining this phenomenon, Hochstein and colleagues2 observed that during the oxidation of TPNH by liver microsomes in the presence of ADP and a small quantity of iron, a substance was formed having properties of malondialdehyde; this indicated that oxidative degradation of polyunsaturated lipids was occurring. The investigations of Orrenius and colleagues3 and Wills4 indicate that the system involves part or all of the drug-metabolizing system. Because the concentrations of TPNH, ADP, and iron required to promote the maximum rate of the microsomal reaction are within the physiological levels existing in the cytosol of the liver cell,5 we undertook to investigate the nature of this phenomenon. The objective of these studies was to determine to what extent membrane-bound electron transport systems involving large free energy changes may promote degradation of lipids in the membranes and associated impairment of enzymic activity. In the course of these studies it was established that dietary a-tocopherol has a regulatory effect on this phenomenon. The results to be presentedindicate that TPNH-dependent electron transport is associated in both microsomes and mitochondria with the production of a highly transient factor possessing the properties of a free radical. This factor apparently promotes the peroxidative chain scission of the polyunsaturated fatty acid (PUFA) moieties of phospholipids in the rnicrosomal and mitochondria1 membranes. I t was also shown that during this process microsomal a-tocopherol is converted to a polar compound and that in mitochondria there is loss of the capacity to carry out oxidation of Krebs cycle intermediates and the associated phosphorylation. This capacity can be restored by the addition of cytochrome c to the assay systems.
