Schulte-Wissermann H, Straub E, Funke P J
Virchows Arch B Cell Pathol. 1977 Feb 8;23(2):163-73. doi: 10.1007/BF02889128.
HgC12-induced renal tubular lesions in the rat present histochemically with a transitory decrease of alkaline phosphatase, adenosinetriphosphatase (ATPase), and leucine-aminopeptidase activity. The toxic alterations of enzyme activity were more pronounced in the pars recta of the proximal tubule and in the loop of Henle, as compared with the tubulus contortus I. L-thyroxine treatment leads to an accelerated reversal of that enzymatic defect, followinga characteristic pattern, and to a differentiating increase of acid phosphatase and ATPase activity in certain parts of the normal renal tubule. The observations are discussed with reference to the specific mode of action of sublimate and l-thyroxine upon the tubular enzymes and to the well-known metabolic and functional influences of thyroid hormone on the kidney.
氯化汞诱导的大鼠肾小管损伤在组织化学上表现为碱性磷酸酶、三磷酸腺苷酶(ATP酶)和亮氨酸氨基肽酶活性的短暂降低。与近曲小管I相比,酶活性的毒性改变在近端小管的直部和髓袢中更为明显。L-甲状腺素治疗导致该酶缺陷按照特征性模式加速逆转,并使正常肾小管某些部位的酸性磷酸酶和ATP酶活性有差异性增加。结合升汞和L-甲状腺素对肾小管酶的特定作用方式以及甲状腺激素对肾脏众所周知的代谢和功能影响对这些观察结果进行了讨论。