Madesh M, Balasubramanian K A
The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College Hospital, Vellore, India.
FEBS Lett. 1997 Aug 18;413(2):269-72. doi: 10.1016/s0014-5793(97)00903-4.
Mitochondrial damage is one of the prominent features of cell death in oxidative stress and related pathological conditions. Alteration in membrane lipid composition may be responsible for the mitochondrial damage. In this study, we have shown that intestinal mitochondria contain an active phospholipase D (PLD) which is activated by oxidants, Ca2+ or polyamines and this results in degradation of phosphatidylethanolamine (PE) and formation of phosphatidic acid (PA). This PLD activity is inhibited by nitric oxide (NO) which prevents the lipid alteration in mitochondria when exposed to these agents. This can be reversed by the NO scavenger, haemoglobin. This suggests that alteration of mitochondrial membrane lipid composition by activation of PLD in certain pathological condition such as oxidative stress may be prevented by the simultaneous presence of nitric oxide.
线粒体损伤是氧化应激及相关病理状态下细胞死亡的显著特征之一。膜脂质组成的改变可能是线粒体损伤的原因。在本研究中，我们发现肠道线粒体含有一种活性磷脂酶D（PLD），它可被氧化剂、Ca2+或多胺激活，导致磷脂酰乙醇胺（PE）降解并形成磷脂酸（PA）。一氧化氮（NO）可抑制这种PLD活性，从而在暴露于这些试剂时防止线粒体中的脂质改变。NO清除剂血红蛋白可逆转这种情况。这表明在某些病理状态如氧化应激下，通过激活PLD改变线粒体膜脂质组成的情况可能会因同时存在一氧化氮而得到预防。
