Xing Ming-luan, Wang Xiao-feng, Zhu Xin, Zhou Xu-dong, Xu Li-hong
Department of Biochemistry and Genetics, School of Medicine, Zhejiang University, Hangzhou 310058, China.
Environ Toxicol. 2009 Oct;24(5):437-45. doi: 10.1002/tox.20446.
The marine toxin okadaic acid (OA) is an apoptosis inducer and a tumor promoter. During recent years, extensive studies have demonstrated that OA can induce apoptosis in a wide variety of cell types. In contrast to the relatively longer incubation time or higher treatment concentrations of OA in apoptosis shown previously, relatively lower concentrations (<or=100 nM) and shorter time (4 h) were designed in the current study to observe the toxic effects of OA in human amniotic cells (FL cells). The present study was undertaken to determine the morphological and biochemical changes of FL cells induced by OA. Results indicated that externalization of phosphatidylserine, cytoskeletal disruption, DNA strand breaks and decrease of Bcl-2 protein expression levels as well as increase of PP2A-A subunit protein were all involved in the apoptosis of FL cells induced by OA. This work not only provided further evidence of apoptosis induced by OA but also suggested that PP2A might play a pivotal role in apoptosis induced by protein phosphatases inhibitors.
海洋毒素冈田酸（OA）是一种凋亡诱导剂和肿瘤促进剂。近年来，大量研究表明，OA可在多种细胞类型中诱导凋亡。与之前显示的OA诱导凋亡相对较长的孵育时间或较高的处理浓度不同，本研究设计了相对较低的浓度（≤100 nM）和较短的时间（4小时）来观察OA对人羊膜细胞（FL细胞）的毒性作用。本研究旨在确定OA诱导的FL细胞的形态学和生化变化。结果表明，磷脂酰丝氨酸外化、细胞骨架破坏、DNA链断裂、Bcl-2蛋白表达水平降低以及PP2A-A亚基蛋白增加均与OA诱导的FL细胞凋亡有关。这项工作不仅为OA诱导凋亡提供了进一步的证据，还表明PP2A可能在蛋白磷酸酶抑制剂诱导的凋亡中起关键作用。
