Hsiao J K, Manji H K, Chen G A, Bitran J A, Risby E D, Potter W Z
Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892.
Life Sci. 1992;50(3):227-33. doi: 10.1016/0024-3205(92)90276-u.
Platelet G proteins were assessed in 7 normal volunteers before and after 14 days of lithium administration at therapeutic plasma levels. Cholera and pertussis toxin catalyzed ADP-ribosylation of platelet membrane proteins were measured by SDS-PAGE. Immunoblotting with specific antibodies was used to measure platelet membrane alpha i content. There was a statistically significant 37% increase in pertussis toxin mediated ADP-ribosylation of a 40,000 Mr protein in platelet membranes after lithium administration, but cholera toxin mediated ADP-ribosylation of a 45,000 Mr protein and alpha i immunoblotting were unchanged by lithium. Increased pertussis toxin stimulated ADP-ribosylation in the absence of changes in alpha i content could be explained by a shift in platelet Gi in favor of its undissociated, inactive form. This would be consistent with increased platelet adenylyl cyclase activity found in these same subjects after lithium.
在7名正常志愿者接受治疗性血浆浓度的锂治疗14天前后，对血小板G蛋白进行了评估。通过SDS - PAGE测定霍乱毒素和百日咳毒素催化的血小板膜蛋白ADP - 核糖基化。使用特异性抗体进行免疫印迹来测量血小板膜αi含量。锂给药后，血小板膜中40,000 Mr蛋白的百日咳毒素介导的ADP - 核糖基化有统计学意义的37%增加，但霍乱毒素介导的45,000 Mr蛋白的ADP - 核糖基化和αi免疫印迹不受锂的影响。在αi含量无变化的情况下，百日咳毒素刺激的ADP - 核糖基化增加可能是由于血小板Gi向有利于其未解离的无活性形式转变所致。这与在这些相同受试者中锂治疗后发现的血小板腺苷酸环化酶活性增加是一致的。
