作者: Ming Wu , Qi Wang , Jiang-Yun Luo , Bo Jiang , Xu-Yun Li
DOI: 10.1016/J.TOXLET.2010.04.014
关键词: Biochemistry 、 NADPH oxidase 、 Phospholipase D 、 Oxidase test 、 Cell culture 、 Molecular biology 、 A549 cell 、 Biology 、 Phosphatidic acid 、 Intracellular 、 Catalase 、 Toxicology 、 General Medicine
摘要: Abstract To determine the role of phospholipase D (PLD) pathway in injury and survival alveolar epithelial cells, A549 cells were exposed to H 2 O (500 μM) which resulted time-dependent bi-phasic increase PLD activity at 5 min 3 h, respectively. n -Butanol (0.5%) inhibited activation, attenuated cell exposure, but enhanced 3 h exposure. This activation was by treatment with catalase (500 units/ml). Exogenous phosphatidic acid mimicked effects diphenyliodonium (NADPH oxidase inhibitor) reversed decline viability induced Propranolol (phosphatidic phospholydrolase quinacrine (phospholipase A2 had weak on -induced injury. We speculate that initiation exposure predominantly results NAPDH mediates injury, turns mediating as attack continues, might be mainly due accumulation intracellular acid.