Merali Z, Singhal R L
Br J Pharmacol. 1976 Aug;57(4):573-9. doi: 10.1111/j.1476-5381.1976.tb10387.x.
Subacute cadmium treatment (CdCl2, 1 mg/kg twice daily for 7 days) in rats disturbs glucose homeostasis as shown by hyperglycemia and decreased glucose tolerance associated with suppression of insulin release, enhancement of hepatic gluconeogenic enzymes and decrease in hepatic glycogen content. 2 Exposure to cadmium increases hepatic cyclic adenosine 3',5'-monophosphate (cyclic AMP) and this is accompanied by stimulation of basal, adrenaline- as well as glucagon-stimulated form(s) of adenylate cyclase. 3 In contrast to cadmium, subacute administration of zinc (ZnCl2, 2 mg/kg twice daily for 7 days) fails to alter the activities of hepatic gluconeogenic enzymes, cyclic AMP synthesis, as well as glucose clearance and insulin release in response to a glucose load. 4 Zinc, when administered at the same time as cadmium, prevents the cadmium-induced lesions in both hepatic and pancreatic functions. 5 The results are discussed in relation to the possible mechanisms of cadmium toxicity and to the role of sulphydryl groups in the protection exercised by zinc.
对大鼠进行亚急性镉处理（氯化镉，每日两次，每次1毫克/千克，共7天）会扰乱葡萄糖稳态，表现为高血糖和葡萄糖耐量降低，同时伴有胰岛素释放受抑制、肝糖异生酶增强以及肝糖原含量减少。2 镉暴露会增加肝脏环磷腺苷（cAMP），同时伴有对基础腺苷酸环化酶、肾上腺素刺激型以及胰高血糖素刺激型腺苷酸环化酶的刺激。3 与镉相反，亚急性给予锌（氯化锌，每日两次，每次2毫克/千克，共7天）不会改变肝糖异生酶的活性、环磷腺苷合成以及葡萄糖负荷后的葡萄糖清除率和胰岛素释放。4 锌与镉同时给药时，可预防镉诱导的肝脏和胰腺功能损伤。5 结合镉毒性的可能机制以及巯基在锌所发挥的保护作用中的作用对结果进行了讨论。
