Vahter M, Marafante E
Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
Biol Trace Elem Res. 1989 Jul-Sep;21:233-9. doi: 10.1007/BF02917258.
Inhibition of the methylation of arsenic in rabbits by ip injection of periodate-oxidized adenosine (PAD) prior to an iv injection of 74As-arsenate (AsV; 0.4 mg As/kg body wt) caused a marked increase in the retention of 74As in both the cellular organelles and the soluble fractions of liver and kidney. One day after exposure, almost 30% of the arsenic in the liver and about 40% of the arsenic in the kidney was recovered in the nuclear fraction. In the liver nuclei, the inhibition of the methylation increased the 74As content of the insoluble fraction and most of this arsenic was protein-bound. The major part of the soluble intranuclear 74As was in the form of AsIII, formed by reduction of the administered AsV. In the liver, PAD also caused a pronounced increase in the 74As content of the microsomal fraction. In the kidneys, where most of the arsenic was present as AsV, there was a marked accumulation of arsenic in the mitochondria.
在静脉注射74As-砷酸盐(AsV;0.4mg As/kg体重)之前,通过腹腔注射高碘酸盐氧化的腺苷(PAD)抑制家兔体内砷的甲基化,导致肝脏和肾脏的细胞器及可溶性部分中74As的保留量显著增加。暴露一天后,肝脏中近30%的砷和肾脏中约40%的砷在核部分被回收。在肝细胞核中,甲基化的抑制增加了不溶性部分的74As含量,且大部分这种砷与蛋白质结合。可溶性核内74As的主要部分是以AsIII的形式存在,它是由所给予的AsV还原形成的。在肝脏中,PAD还使微粒体部分的74As含量显著增加。在肾脏中,大部分砷以AsV的形式存在,线粒体中有明显的砷积累。