Machida K, Tanaka T
Department of Biology, Graduate School of Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka, Japan.
FEBS Lett. 1999 Nov 26;462(1-2):108-12. doi: 10.1016/s0014-5793(99)01506-9.
An isoprenoid farnesol (FOH) inhibited cellular oxygen consumption and induced mitochondrial generation of reactive oxygen species (ROS) in cells of Saccharomyces cerevisiae in correlation with hyperpolarization of the mitochondrial transmembrane potential (mtDeltaPsi). The FOH-induced events were coordinately abolished with the F(1)-ATPase inhibitor sodium azide as well as the F(0)F(1)-ATPase inhibitor oligomycin, suggesting the dependence of ROS generation on mtDeltaPsi hyperpolarization mediated by the proton pumping function of F(0)F(1)-ATPase as a result of ATP hydrolysis. The role of F(1)-ATPase activity in mtDeltaPsi hyperpolarization was supported by the intracellular depletion of ATP in FOH-treated cells and its protection with sodium azide. An indirect mechanism was suggested to exist in the regulation of F(0)F(1)-ATPase by FOH to accelerate its ATP-hydrolyzing activity.
类异戊二烯法尼醇（FOH）抑制酿酒酵母细胞中的细胞耗氧量，并诱导线粒体活性氧（ROS）生成，这与线粒体跨膜电位（mtΔΨ）的超极化相关。FOH诱导的这些事件被F1-ATP酶抑制剂叠氮化钠以及F0F1-ATP酶抑制剂寡霉素协同消除，这表明ROS生成依赖于因ATP水解通过F0F1-ATP酶的质子泵功能介导的mtΔΨ超极化。FOH处理细胞中ATP的细胞内耗竭及其被叠氮化钠保护，支持了F1-ATP酶活性在mtΔΨ超极化中的作用。提示存在一种由FOH调节F0F1-ATP酶以加速其ATP水解活性的间接机制。
