Enhanced lysosomal phospholipid degradation and lysophospholipid production due to free radicals.

Enhanced lysosomal phospholipid degradation and lysophospholipid production due to free radicals.
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由于自由基,增强了溶酶体磷脂的降解和溶酶体磷脂的产生。

DOI:
10.1016/0006-291x(84)90941-0
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发表时间:
1984
影响因子:
3.1
通讯作者:
Mak,IT
Mak,IT
中科院分区:
生物学4区
文献类型:
--
作者:
Weglicki,WB;Dickens,BF;Mak,IT

文献摘要

被引文献

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为了探讨过氧化脂质可能成为内源性磷脂酶的首选底物的假设,我们通过添加外源自由基生成系统[二羟基富马酸+Fe3+-ADP]来损伤肝脏溶酶体,该系统在pH为6.0时迅速裂解肝脏溶酶体,30min时变化最大。丙二醛[MDA]的产生迅速趋于平稳。在20min时,磷脂酰乙醇胺[PE]的降解率为52%,而磷脂酰胆碱[PC]的降解率为17%。神经鞘磷脂和中性脂类没有下降。最有趣的是,在孵育10分钟和20分钟后,溶菌素PC显著增加[329%;p<0.05]和[381%;p<0.01];溶菌素PE产量在20分钟达到显著水平[766%;p<0.05]。这种增加的溶质PC和溶质PE的产生提示了一种新的机制,即在没有添加钙的情况下,在中等酸性的pH下,增加了缺血期间两亲性脂质的产生。
To pursue the hypothesis that peroxidized lipids may become preferred substrates for endogenous phospholipases, we injured hepatic lysosomes by adding an exogenous free radical generating system [dihydroxyfumurate + Fe3+-ADP]; this system rapidly lysed hepatic lysosomes at pH 6.0, with maximal changes at 30 min. The production of malondialdehyde [MDA] plateaued rapidly. At 20 min the degradation of phosphatidylethanolamine [PE] was greater than phosphatidylcholine [PC]: 52% and 17%, respectively. Sphingomyelin and neutral lipids did not decrease. Most interesting was the significant increase of lysoPC [329%; p < 0.05] at 10 min and [381%; p < 0.01] after 20 min of incubation; lysoPE production became significant [766%; p < 0.05] at 20 min. This enhanced production of lysoPC and lysoPE suggests a new mechanism to increase the production of amphiphilic lipids during ischemia, that is active at moderately acid pH without added calcium.