Machu T, Woodward J J, Leslie S W
University of Texas, College of Pharmacy, Austin 78712.
Alcohol. 1989 Nov-Dec;6(6):431-6. doi: 10.1016/0741-8329(89)90047-5.
The effects of ethanol on ATP-dependent Ca2+ uptake and inositol 1,4,5-trisphosphate (Ins-P3)-induced Ca2+ release were assessed in rat cerebellar and cortical microsomes. Ins-P3, 0.2-10 microM, released 7-14% of ATP loaded microsomal Ca2+ stores after a 15-sec exposure. Ethanol, 250-750 mM, added after ATP-dependent loading, significantly released microsomal Ca2+ stores, and the amount released was additive to that seen with Ins-P3 alone. The presence of ethanol, 250-750 mM, during the ATP-dependent loading period, resulted in decreased Ca2+ uptake that correlated with decreases in Ins-P3-induced Ca2+ release. Chronic ethanol treatment failed to produce any alterations in ethanol's ability to promote Ca2+ release or to inhibit ATP-dependent Ca2+ uptake. Furthermore, Ins.-P3-induced Ca2+ release was not altered by chronic ethanol treatment. These results suggest that Ins-P3 sensitive Ca2+ stores are resistant to pharmacologically relevant concentrations of ethanol, and do not appear to be involved in the chronic cellular effects of ethanol.
在大鼠小脑和皮质微粒体中评估了乙醇对ATP依赖性Ca2+摄取及肌醇1,4,5-三磷酸（Ins-P3）诱导的Ca2+释放的影响。15秒暴露后，0.2 - 10微摩尔的Ins-P3释放了ATP负载微粒体Ca2+储存量的7 - 14%。在ATP依赖性负载后添加250 - 750毫摩尔的乙醇，显著释放了微粒体Ca2+储存量，且释放量与单独使用Ins-P3时所见的量具有加和性。在ATP依赖性负载期间存在250 - 750毫摩尔的乙醇，导致Ca2+摄取减少，这与Ins-P3诱导的Ca2+释放减少相关。慢性乙醇处理未能使乙醇促进Ca2+释放或抑制ATP依赖性Ca2+摄取的能力产生任何改变。此外，慢性乙醇处理未改变Ins-P3诱导的Ca2+释放。这些结果表明，Ins-P3敏感的Ca2+储存对药理学相关浓度的乙醇具有抗性，且似乎不参与乙醇的慢性细胞效应。
