Rottenberg H, Marbach M
Pathology Department, Hahnemann University, Philadelphia, PA 19102.
Life Sci. 1991;48(10):987-94. doi: 10.1016/0024-3205(91)90364-h.
Ethanol, at low concentrations, specifically stimulates the Na(+)-dependent Ca2(+)-efflux in brain mitochondria. In addition, at higher concentrations, ethanol inhibits the Na(+)-independent Ca2(+)-efflux. The electrogenic Ca(+)-uptake system is not affected by ethanol. The specific stimulation of Na+/Ca2+ exchange reaches a maximum of 60% stimulation, with half-maximal stimulation at 130 mM ethanol. The inhibition of the Na(+)-independent efflux is proportional to the ethanol concentration, becoming significant only above 200 mM, with 50% inhibition at 0.5 M. The inhibition of the Na(+)-independent efflux is, in large part, due to an inhibition of the activation of the Cyclosporin-sensitive pore. Long-term ethanol-feeding had no effect on the Ca2+ transport systems and their sensitivity to acute ethanol treatment. It is suggested that the stimulation of the Na(+)-dependent Ca2(+)-efflux, which is the dominant Ca2+ efflux pathway in brain mitochondria, contributes to the intoxicating effects of ethanol.
低浓度乙醇能特异性刺激脑线粒体中依赖钠的钙离子外流。此外,高浓度乙醇会抑制不依赖钠的钙离子外流。电生性钙离子摄取系统不受乙醇影响。钠/钙离子交换的特异性刺激作用最大可达60%的刺激程度,在130 mM乙醇浓度时达到半最大刺激。不依赖钠的外流抑制作用与乙醇浓度成正比,仅在200 mM以上才显著,在0.5 M时抑制率达50%。不依赖钠的外流抑制作用在很大程度上是由于对环孢菌素敏感孔道激活的抑制。长期给予乙醇对钙离子转运系统及其对急性乙醇处理的敏感性没有影响。有人提出,依赖钠的钙离子外流的刺激作用(这是脑线粒体中主要的钙离子外流途径)促成了乙醇的中毒作用。