a Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas , Universidade Federal de Santa Maria , Santa Maria , RS , Brazil.
c Departamento de Ciências da Saúde , Universidade Federal de Santa Maria , Palmeira das Missões , RS , Brazil.
J Toxicol Environ Health A. 2018;81(14):633-644. doi: 10.1080/15287394.2018.1474153. Epub 2018 May 29.
Mercury (Hg), a divalent metal, produces adverse effects predominantly in the renal and central nervous systems. The aim of this study was to determine the effectiveness of copper (Cu) in prevention of mercuric mercury (Hg)-mediated toxic effects as well as the role metallothioneins (MT) play in this protective mechanism in young rats. Wistar rats were treated subcutaneously with saline (Sal) or CuCl.2HO (Cu 2.6 mg/kg/day) from 3 to 7 days old and with saline or HgCl (Hg 3.7 mg/kg/day) from 8 to 12 days old. The experimental groups were (1) Sal-Sal, (2) Cu-Sal, (3) Sal-Hg, and (4) Cu-Hg. MTs and metal contents were determined at 13 and 33 days of age. Porphobilinogen synthase (PBG-synthase) activity as well as renal and hepatic parameters were measured at 33 days. At 13 day, Hg exposure increased hepatic MT, Hg, zinc (Zn) and iron (Fe) levels, in kidney elevated Cu and Hg and decreased renal Fe concentrations, accompanied by elevated blood Hg levels. At 33 days, Hg exposure inhibited renal PBG-synthase activity, increased serum urea levels and lowered Fe and Mg levels. Copper partially prevented the rise in blood Hg and liver Fe noted at 13 days; and completely blocked urea rise and diminished renal PBG-synthase activity inhibition at 33 days. In 13-day-old rats, Cu exposure redistributed the Hg in the body, decreasing hepatic and blood levels while increasing renal levels, accompanied by elevated renal and hepatic MT levels in Hg-exposed animals. These results suggest that hepatic MT might bind to hepatic and blood Hg for transport to the kidney in order to be excreted.
MT: metallothioneins; PBG-synthase: porphobilinogen synthase.
汞（Hg）是一种二价金属，主要对肾脏和中枢神经系统产生不良影响。本研究旨在确定铜（Cu）在预防汞（Hg）介导的毒性作用中的有效性，以及金属硫蛋白（MT）在年轻大鼠这种保护机制中的作用。Wistar 大鼠从 3 至 7 天大时皮下接受生理盐水（Sal）或 CuCl.2HO（Cu 2.6mg/kg/天）治疗，从 8 至 12 天大时接受生理盐水或 HgCl（Hg 3.7mg/kg/天）治疗。实验分组如下：（1）Sal-Sal，（2）Cu-Sal，（3）Sal-Hg，和（4）Cu-Hg。在 13 和 33 天大时测定 MT 和金属含量。在 33 天大时测定苯丙氨酸解氨酶（PBG-合酶）活性以及肾脏和肝脏参数。在 13 天，Hg 暴露增加了肝脏 MT、Hg、锌（Zn）和铁（Fe）水平，在肾脏增加了 Cu 和 Hg 并降低了肾脏 Fe 浓度，同时伴有血 Hg 水平升高。在 33 天，Hg 暴露抑制了肾脏 PBG-合酶活性，增加了血清尿素水平并降低了 Fe 和 Mg 水平。Cu 部分阻止了在 13 天观察到的血 Hg 和肝 Fe 升高；完全阻断了 33 天尿素升高和减少了肾脏 PBG-合酶活性抑制。在 13 天大的大鼠中，Cu 暴露重新分配了体内的 Hg，降低了肝和血中的水平，同时增加了肾中的水平，伴随着 Hg 暴露动物的肾和肝 MT 水平升高。这些结果表明，肝 MT 可能与肝和血 Hg 结合，以便将其运输到肾脏进行排泄。
MT：金属硫蛋白；PBG-合酶：苯丙氨酸解氨酶。
