Wetzels J F, Wang X, Gengaro P E, Nemenoff R A, Burke T J, Schrier R W
Department of Medicine, University of Colorado School of Medicine, Denver 80262.
Am J Physiol. 1993 Jan;264(1 Pt 2):F94-9. doi: 10.1152/ajprenal.1993.264.1.F94.
We studied the effects of glycine (2 mM) on hypoxia-induced changes in phospholipids and fatty acids in isolated rat proximal tubules. In this preparation, 25 min of hypoxia caused cell injury, as reflected by the release of lactate dehydrogenase (LDH) (13.1 +/- 0.8 vs. 43.5 +/- 3.2%; P < 0.01). Hypoxia caused increases in fatty acids and in lysophospholipids. Glycine prevented the hypoxia-induced cell injury (LDH 13.1 +/- 0.8 vs. 11 +/- 0.7%; not significant) but did not attenuate the increases in fatty acids or lysophospholipids. In additional experiments, the effects of glycine on phospholipid changes and cell injury induced by exogenous phospholipase A2 (PLA2) were studied. PLA2 caused dramatic increases in fatty acids and lysophospholipids and mild cell injury; these effects were not influenced by glycine. In contrast, glycine attenuated increases in LDH release induced by exposing the tubules to exogenous arachidonic acid. In conclusion, glycine does not prevent the phospholipid degradation induced by either exogenous PLA2 or hypoxia in isolated proximal tubules and yet affords protection against hypoxia and exogenous arachidonic acid.
我们研究了甘氨酸(2 mM)对离体大鼠近端肾小管中磷脂和脂肪酸的缺氧诱导变化的影响。在此实验准备中,25分钟的缺氧导致细胞损伤,这通过乳酸脱氢酶(LDH)的释放得以体现(13.1±0.8%对43.5±3.2%;P<0.01)。缺氧导致脂肪酸和溶血磷脂增加。甘氨酸可防止缺氧诱导的细胞损伤(LDH为13.1±0.8%对11±0.7%;无显著差异),但并未减弱脂肪酸或溶血磷脂的增加。在另外的实验中,研究了甘氨酸对外源性磷脂酶A2(PLA2)诱导的磷脂变化和细胞损伤的影响。PLA2导致脂肪酸和溶血磷脂显著增加以及轻度细胞损伤;这些效应不受甘氨酸影响。相反,甘氨酸减弱了将肾小管暴露于外源性花生四烯酸所诱导的LDH释放增加。总之,甘氨酸不能防止外源性PLA2或缺氧在离体近端肾小管中诱导的磷脂降解,但却能提供针对缺氧和外源性花生四烯酸的保护作用。