Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Av. Prof. Lineu Prestes, 1524, 05508-900 São Paulo, Brazil.
Toxicol In Vitro. 2011 Dec;25(8):2140-6. doi: 10.1016/j.tiv.2011.06.011. Epub 2011 Jun 24.
The effects of stearic (saturated) or oleic (monounsaturated) acids and their combination with ω-3 and ω-6 polyunsaturated fatty acids (PUFA) on death of endothelial cells (ECV-304 cell line) were investigated. We examined: loss of plasma membrane integrity, DNA fragmentation, accumulation of neutral lipids (NL) and release of reactive oxygen species (ROS). The fatty acids studied were: stearic (SA), oleic (OA), docosahexaenoic (DHA), eicosapentaenoic (EPA), linoleic (LA) and gamma-linolenic (γA) acids. SA at 150 μM induced cell death, did not lead to accumulation of NL and raised the release of ROS. ω-3 PUFA decreased ROS production, increased NL content but did not protect against ECV-304 cell death induced by SA. ω-6 PUFA inhibited SA-induced cell death, increased NL content and decreased ROS production. OA caused cell death but did not increase NL content and ROS production even at 300 μM. ω-3 and ω-6 FA associated with OA further increased cell death with no change in ROS production and NL content. Concluding, ω-6 PUFA had a greater protective effect than ω-3 PUFA on the deleterious effects caused by SA whereas OA had low cytotoxicity but, when associated with PUFA, presented marked toxic effects on ECV-304 endothelial cells.
研究了硬脂酸(饱和)或油酸(单不饱和)酸及其与 ω-3 和 ω-6 多不饱和脂肪酸(PUFA)的组合对内皮细胞(ECV-304 细胞系)死亡的影响。我们检查了:质膜完整性丧失、DNA 片段化、中性脂质(NL)积累和活性氧物种(ROS)的释放。研究的脂肪酸有:硬脂酸(SA)、油酸(OA)、二十二碳六烯酸(DHA)、二十碳五烯酸(EPA)、亚油酸(LA)和γ-亚麻酸(γA)。150 μM 的 SA 诱导细胞死亡,不会导致 NL 积累,并增加 ROS 的释放。ω-3 PUFA 降低 ROS 产生,增加 NL 含量,但不能防止 SA 诱导的 ECV-304 细胞死亡。ω-6 PUFA 抑制 SA 诱导的细胞死亡,增加 NL 含量并降低 ROS 产生。OA 引起细胞死亡,但即使在 300 μM 时也不会增加 NL 含量和 ROS 产生。与 OA 相关的 ω-3 和 ω-6 FA 进一步增加了细胞死亡,而 ROS 产生和 NL 含量没有变化。总之,ω-6 PUFA 对 SA 引起的有害作用的保护作用大于 ω-3 PUFA,而 OA 的细胞毒性较低,但与 PUFA 结合时,对 ECV-304 内皮细胞表现出明显的毒性作用。