Kingsley B S, Frazier J M
Am J Physiol. 1979 Mar;236(3):C139-43. doi: 10.1152/ajpcell.1979.236.3.C139.
The hypothesis that one component of cadmium uptake by rat hepatocytes involves a mediated transport pathway normally operative for zinc transport was tested in the isolated perfused rat liver preparation. Excess zinc in the perfusion medium suppressed cadmium uptake as indicated by the decrease in the normalized clearance (initial clearance divided by liver weight) from 0.340 +/- 0.019 (ml/min)/g in the presence of normal zinc concentrations (Zn:Cd molar ratio, 1.6) to 0.138 +/- 0.017 (ml/min)/g (Zn:Cd molar ratio, 13.0). In excess-zinc control experiments (no cadmium present) little zinc is accumulated by the liver, apparently due to competition between intrahepatic and extracellular binding. Exposure to cadmium increases both zinc secretion into the perfusion medium and biliary excretion of zinc. The effect at the sinusoidal membrane is probably a result of both the blockage of zinc resorption during cadmium uptake and the displacement of intrahepatic zinc. The effect on biliary excretion of zinc is due solely to displacement of intrahepatic zinc. These results are consistent with the proposed hypothesis for cadmium transport.
在离体灌注大鼠肝脏标本中，对大鼠肝细胞摄取镉的一种成分涉及通常用于锌转运的介导转运途径这一假说进行了检验。灌注培养基中过量的锌抑制了镉的摄取，正常锌浓度（锌：镉摩尔比为1.6）下归一化清除率（初始清除率除以肝脏重量）从0.340±0.019（毫升/分钟）/克降至0.138±0.017（毫升/分钟）/克（锌：镉摩尔比为13.0）就表明了这一点。在过量锌对照实验（无镉存在）中，肝脏积累的锌很少，这显然是由于肝内和细胞外结合之间的竞争所致。接触镉会增加锌向灌注培养基中的分泌以及锌的胆汁排泄。在肝血窦膜处的这种作用可能是镉摄取期间锌重吸收受阻和肝内锌被取代这两者的结果。对锌胆汁排泄的作用仅归因于肝内锌的被取代。这些结果与所提出的镉转运假说一致。
