Faculty of Medicine, University of Tsukuba, 1-1-1 Ten-nohdai, Tsukuba, Ibaraki 305-8573, Japan.
J Clin Biochem Nutr. 2013 Sep;53(2):75-80. doi: 10.3164/jcbn.13-32. Epub 2013 Aug 31.
Alcohol/ethanol has been reported to derived necrosis and apoptosis with an oxidative stress in gastric mucosal cells. However the clear evidence for reactive oxygen species (ROS) generation by alcohol in gastric cells in vitro is none. In this study, we elucidated ethanol is an oxidative stress inducer on rat gastric epithelial cells by electron paramagnetic resonance measurement in living cells. We also confirmed whether ethanol-induced cellular ROS was derived from mitochondria or not. The results of cellular ROS determination showed that an increment of cellular ROS was shown for 15 min from exposing 1% (v/v) ethanol. Lipid peroxidation in cellular membrane also induced by 1% ethanol and the tendency is same in the results of cellular ROS determination. JC-1 stained showed the decrement of mitochondrial membrane potential. Additionally the localization of cellular ROS coincided with mitochondria. These results indicated that ethanol is not merely a necrotizing factor for gastric epithelial cells, but also an oxidative stress inducer via injured mitochondria.
酒精/乙醇已被报道在胃黏膜细胞中产生氧化应激导致坏死和凋亡。然而，在体外胃细胞中酒精产生活性氧（ROS）的明确证据是没有的。在这项研究中，我们通过活细胞中的电子顺磁共振测量阐明了乙醇是一种诱导大鼠胃上皮细胞氧化应激的物质。我们还证实了乙醇诱导的细胞内 ROS 是否来自线粒体。细胞内 ROS 测定的结果表明，暴露于 1%（v/v）乙醇 15 分钟后，细胞内 ROS 增加。1%乙醇也诱导了细胞膜的脂质过氧化，细胞内 ROS 测定的结果也有同样的趋势。JC-1 染色显示线粒体膜电位下降。此外，细胞内 ROS 的定位与线粒体一致。这些结果表明，乙醇不仅是胃上皮细胞的坏死因素，而且还通过损伤的线粒体诱导氧化应激。
