Roychoudhury S, Chakraborti T, Ghosh J J, Ghosh S K, Chakraborti S
Department of Biochemistry and Biophysics, University of Kalyani, West Bengal, India.
Indian J Biochem Biophys. 1996 Jun;33(3):218-22.
Treatment of bovine pulmonary artery smooth muscle mitochondria with H2O2 stimulated oxidation of GSH and NAD(P)H along with an increase in Ca2+ release. Addition of oxaloacetate to mitochondrial suspension stimulated Ca2+ release and oxidation of NAD(P)H while GSH level remained unchanged. Subsequently, addition of beta-hydroxybutyrate which reduced mitochondrial pyridine nucleotides caused reuptake of the released Ca2+ without causing appreciable alteration of GSH level. Treatment of the mitochondria with 1,3-bis(2-dichloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase, significantly decreased GSH level without producing discernible change in Ca2+ release and NAD(P)H oxidation.
用H2O2处理牛肺动脉平滑肌线粒体,刺激了谷胱甘肽(GSH)和烟酰胺腺嘌呤二核苷酸(磷酸)(NAD(P)H)的氧化,同时钙离子(Ca2+)释放增加。向线粒体悬浮液中添加草酰乙酸刺激了Ca2+释放和NAD(P)H的氧化,而GSH水平保持不变。随后,添加β-羟基丁酸酯可降低线粒体吡啶核苷酸,导致释放的Ca2+重新摄取,而不会引起GSH水平的明显改变。用谷胱甘肽还原酶抑制剂1,3-双(2-二氯乙基)-1-亚硝基脲(BCNU)处理线粒体,显著降低了GSH水平,而Ca2+释放和NAD(P)H氧化没有明显变化。