Masuda Y, Ozaki M, Aoki S
Division of Toxicology, Niigata College of Pharmacy, Japan.
FEBS Lett. 1993 Nov 8;334(1):109-13. doi: 10.1016/0014-5793(93)81692-s.
Tert-butyl hydroperoxide (BHP), hydrogen peroxide and diamide caused a rapid and simultaneous release of glutathione disulfide (GSSG) and K+ in the isolated perfused rat liver. Both BHP-induced effluxes were suppressed by prior depletion of hepatic glutathione, but not by co-infusion of desferrioxamine which prevented lipid peroxidation and cell death. High K+ media decreased the GSSG efflux even though hepatic GSSG levels remained high. The GSSG and K+ effluxes were repeatable if cellular K+ recovered after a short BHP exposure. Ouabain inhibited the K+ re-uptake and decreased the response to repeated BHP challenge. Thus, sinusoidal efflux of GSSG under oxidative stress may be driven by a K+ gradient.
叔丁基过氧化氢（BHP）、过氧化氢和二酰胺可使离体灌注大鼠肝脏中谷胱甘肽二硫化物（GSSG）和钾离子（K⁺）迅速同时释放。BHP诱导的两种流出均被预先耗尽肝脏谷胱甘肽所抑制，但共同输注去铁胺（可防止脂质过氧化和细胞死亡）则不能抑制。高钾培养基降低了GSSG流出，尽管肝脏GSSG水平仍很高。如果在短暂暴露于BHP后细胞内钾离子恢复，GSSG和K⁺流出是可重复的。哇巴因抑制K⁺再摄取并降低对重复BHP刺激的反应。因此，氧化应激下GSSG的窦状隙流出可能由K⁺梯度驱动。
