Department of Pharmacology, University Medical School of Pécs, Szigeti út 12, H-7643 Pécs, Hungary.
Environ Toxicol Pharmacol. 1998 Mar;5(2):89-99. doi: 10.1016/s1382-6689(97)10008-4.
The interrelationship between the biliary excretion of exogenous group Va-metalloids (arsenic, antimony and bismuth) and selenium, as well as endogenous glutathione has been studied in rats injected intravenously with sodium selenite and one of the group Va-metalloids. Arsenic, antimony and bismuth appeared in the bile of rats together with large amounts of non-protein thiols (NPSH, representing glutathione and its SH-containing degradation products) and, with the exception of bismuth, they caused choleresis. Significant interactions were observed in the hepatobiliary disposition between selenium and each of the group Va-metalloids, however, their outcomes were not uniform. When coadministered with sodium arsenite or arsenate, selenite enhanced the initial biliary excretion of arsenic 2- and 8-fold, respectively, without further increasing the concomitant excretion of NPSH or the choleretic effect of arsenicals. However, selenite augmented neither the excretion of antimony or bismuth, nor the simultaneous biliary release of NPSH. In turn, arsenite, arsenate and antimony potassium tartrate increased the initial biliary excretion of selenium more than 10-fold and enhanced the accumulation of selenium in blood (exclusively in the erythrocytes). In contrast, administration of bismuth ammonium citrate diminished both the biliary excretion and the erythrocytic accumulation of selenium, while causing retention of selenium in the blood plasma. In rats receiving arsenic or antimony with selenite, the time courses of the biliary excretion of these group Va-metalloids, selenium and NPSH were similar. It is hypothesised that incorporation of selenol metabolites of selenite into the glutathione complexes of arsenic and antimony, resulting in cholephilic ternary complexes, accounts for the arsenic- and antimony-induced augmentation of the hepatobiliary transport of selenium. However, additional chemical and/or dispositional mechanisms are thought to be responsible for the selenite-induced increase in biliary excretion of arsenic.
已经在静脉注射亚硒酸钠和一种 Va 族金属（砷、锑和铋）的大鼠中研究了外源性 Va 族金属（砷、锑和铋）和硒之间以及内源性谷胱甘肽之间的相互关系。砷、锑和铋与大量非蛋白巯基（NPSH，代表谷胱甘肽及其含 SH 的降解产物）一起出现在大鼠的胆汁中，并且除了铋之外，它们还引起胆汁分泌。在硒与 Va 族金属中的每一种之间的肝胆处置中观察到显著的相互作用，但是它们的结果并不一致。当与亚砷酸钠或砷酸盐一起给予时，亚硒酸钠分别增强了砷的初始胆汁排泄 2 倍和 8 倍，而没有进一步增加同时排泄的 NPSH 或砷剂的利胆作用。然而，亚硒酸钠既没有增加锑或铋的排泄，也没有同时增加 NPSH 的胆汁释放。相反，砷酸盐、砷酸盐和酒石酸锑钾使硒的初始胆汁排泄增加了 10 倍以上，并增加了硒在血液中的积累（仅在红细胞中）。相比之下，给予柠檬酸铵铋既减少了硒的胆汁排泄和红细胞积累，又导致了硒在血浆中的保留。在给予大鼠砷或锑与亚硒酸钠的情况下，这些 Va 族金属、硒和 NPSH 的胆汁排泄时间过程相似。据推测，亚硒酸盐的硒醇代谢物掺入砷和锑的谷胱甘肽复合物中，导致亲胆的三元复合物，这解释了砷和锑诱导的硒的肝胆转运增强。然而，认为其他化学和/或处置机制负责亚硒酸盐诱导的胆汁中砷排泄增加。
