Tan T M, Sin Y M, Wong K P
Department of Biochemistry, National University of Singapore.
Toxicology. 1990 Oct;64(1):81-7. doi: 10.1016/0300-483x(90)90101-l.
Administration of mercuric chloride to young adult mice produced a significant increase in the activity of renal UDP-glucuronyltransferase (UDPGT) measured with harmol as the acceptor substrate. This was observed 10 days after a daily oral dose of HgCl2 (6 micrograms Hg2+/g body wt.). The increase in UDPGT activity was correlated with an accumulation of mercury in the renal tissues and was accompanied by an increase in the apparent Vmax of the glucuronidation reaction without a change in the apparent Km values for harmol or UDPGA. Parallel studies with mercuric sulfide however showed negligible retention of mercury in both the liver or kidney nor was there any change in UDPGT activity compared to control values. The difference in solubilities of the two mercuric salts may be responsible for this observation. The possible mode of activation of UDPGT by mercury treatment is discussed.
给成年小鼠施用氯化汞后，以哈尔醇作为受体底物测定的肾UDP-葡萄糖醛酸基转移酶（UDPGT）活性显著增加。在每日口服剂量的HgCl2（6微克Hg2+/克体重）10天后观察到这种情况。UDPGT活性的增加与肾组织中汞的积累相关，并伴随着葡萄糖醛酸化反应的表观Vmax增加，而哈尔醇或UDPGA的表观Km值没有变化。然而，用硫化汞进行的平行研究表明，肝脏或肾脏中汞的保留量可忽略不计，与对照值相比，UDPGT活性也没有任何变化。两种汞盐溶解度的差异可能是造成这一观察结果的原因。文中讨论了汞处理激活UDPGT的可能方式。
