Komsta-Szumska E, Miller D R
Toxicol Ind Health. 1986 Dec;2(4):337-49. doi: 10.1177/074823378600200401.
Cadmium chloride (Cd) was injected s.c. into male rats at a dose rate of 3 mg Cd/kg 3 times a week for 4 weeks. The animals were maintained for administration of methylmercury (203 Hg) chloride at a dose of 3 mg CH3Hg/kg given p.o. 3 times a week for 2 weeks, followed by 3 weeks of recovery period. Animals were sacrificed 24 h after the final dose of MeHg, or 5 weeks after cessation of Cd administration. Cd-pretreatment significantly decreased total Hg concentration in the kidney and RBC and almost completely inhibited demethylation of MeHg in the kidney (from 32% to 3% of inorganic Hg). Cd-pretreatment did not affect urinary excretion of total Hg, but significantly increased daily excretion of total Hg in feces. MeHg given alone significantly increased renal but not hepatic copper levels and decreased copper in the plasma and brain. In Cd-pretreated rats, both renal and hepatic copper concentration were in the normal ranges. Zinc levels in Cd-pretreated rats significantly increased in the kidney, liver and brain but decreased in plasma (compared to control and MeHg-alone treated animals). From these results it can be concluded that Cd-pretreatment may decrease MeHg toxicity by increasing the fecal mercury excretion and by inhibiting the formation of inorganic mercury in the kidney, which is a more potent renal toxin than MeHg.
将氯化镉（Cd）以3毫克Cd/千克的剂量皮下注射到雄性大鼠体内，每周3次，持续4周。之后给这些动物口服氯化甲基汞（203Hg），剂量为3毫克CH3Hg/千克，每周3次，持续2周，随后有3周的恢复期。在末次给予甲基汞后24小时，或停止给予镉后5周处死动物。镉预处理显著降低了肾脏和红细胞中的总汞浓度，并几乎完全抑制了肾脏中甲基汞的去甲基化（从无机汞的32%降至3%）。镉预处理不影响总汞的尿排泄，但显著增加了粪便中总汞的每日排泄量。单独给予甲基汞显著增加了肾脏而非肝脏中的铜水平，并降低了血浆和脑中的铜含量。在镉预处理的大鼠中，肾脏和肝脏中的铜浓度均在正常范围内。镉预处理大鼠的肾脏、肝脏和脑中的锌水平显著升高，但血浆中的锌水平降低（与对照组和单独给予甲基汞处理的动物相比）。从这些结果可以得出结论，镉预处理可能通过增加粪便汞排泄和抑制肾脏中无机汞的形成来降低甲基汞的毒性，无机汞是一种比甲基汞更强的肾脏毒素。
