Grynberg A, Nalbone G, Degois M, Leonardi J, Athias P, Lafont H
INRA, Dijon, France.
Biochim Biophys Acta. 1988 Jan 19;958(1):24-30. doi: 10.1016/0005-2760(88)90242-1.
Phospholipid catabolism is thought to be one of the critical events in membrane injury during heart ischemia. In this work, the enzymes involved in phospholipid metabolism were studied in purified cultured ventricular myocytes in normoxic and hypoxic conditions. Purified ventricular myocytes exhibited an alkaline phospholipase A activity which had sn-2 specificity and which was calcium dependent, and an acid phospholipase A activity with sn-1 specificity. These cells also exhibited lysophospholipase and acyl-CoA/lysophosphatidylcholine acyltransferase activities. Oxygen deprivation of the myocardial cells for 4 h resulted in a sharp reduction of both phospholipase A2 and A1 activities. The activities of the other lipolytic enzymes were unaffected by hypoxia. Although hypoxia resulted in a marked increase of lactate dehydrogenase leakage in the bathing fluid, no additional release of the lipolytic enzymes and mitochondrial enzyme was observed. However, we noted an important alkaline phospholipase A2 leakage during normoxia. It is suggested that ventricular myocytes, under hypoxia, tend to prevent phospholipid degradation by reducing their phospholipase A activities.
磷脂分解代谢被认为是心脏缺血期间膜损伤的关键事件之一。在这项研究中，我们在常氧和低氧条件下，对纯化培养的心室肌细胞中参与磷脂代谢的酶进行了研究。纯化的心室肌细胞表现出具有sn-2特异性且依赖钙的碱性磷脂酶A活性，以及具有sn-1特异性的酸性磷脂酶A活性。这些细胞还表现出溶血磷脂酶和酰基辅酶A/溶血磷脂酰胆碱酰基转移酶活性。心肌细胞缺氧4小时导致磷脂酶A2和A1活性急剧降低。其他脂解酶的活性不受缺氧影响。虽然缺氧导致浴液中乳酸脱氢酶泄漏显著增加，但未观察到脂解酶和线粒体酶的额外释放。然而，我们注意到在常氧期间有重要的碱性磷脂酶A2泄漏。这表明在缺氧条件下，心室肌细胞倾向于通过降低其磷脂酶A活性来防止磷脂降解。
