Masini A, Botti B, Ceccarelli D, Muscatello U, Vannini V
Biochim Biophys Acta. 1986 Nov 5;852(1):19-24. doi: 10.1016/0005-2728(86)90051-4.
Addition of 1,2-dibromoethane to rat-liver mitochondria induces a concentration-dependent depletion of mitochondrial glutathione. This event seems to be associated with the induction of Ca2+ release from mitochondria pre-loaded with a low pulse of Ca2+. The enhancement of the energy-dissipating process to reaccumulate the released Ca2+ ('Ca2+ cycling') results in a progressive drop of membrane potential. Addition of EGTA (ethyleneglycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid), when the membrane potential has reached the lowest level, restitutes it to a normal value. All these findings and the observation that Ca2+ release also occurs under non cycling conditions (e.g., in the presence of ruthenium red) suggest that 1,2-dibromoethane induces a Ca2+ efflux by activating a selective pathway which is sensitive to critical sulfhydryl groups.
向大鼠肝脏线粒体中添加1,2 - 二溴乙烷会导致线粒体谷胱甘肽浓度依赖性耗竭。这一事件似乎与预先加载低剂量钙离子脉冲的线粒体中钙离子释放的诱导有关。为了重新积累释放的钙离子（“钙离子循环”）而增强的能量耗散过程会导致膜电位逐渐下降。当膜电位达到最低水平时添加乙二醇双（β - 氨基乙基醚）- N,N,N',N'-四乙酸（EGTA），可使其恢复到正常值。所有这些发现以及在非循环条件下（例如在钌红存在的情况下）也会发生钙离子释放的观察结果表明，1,2 - 二溴乙烷通过激活对关键巯基敏感的选择性途径诱导钙离子外流。
