Dock L, Mottet K, Vahter M
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Pharmacol Toxicol. 1994 Mar;74(3):158-61. doi: 10.1111/j.1600-0773.1994.tb01092.x.
Exposure to mercuric compounds at high dose levels has previously been shown to alter the integrity and function of the blood-brain barrier in laboratory animals. In the present study, we have investigated the distribution of intravenously administered inorganic 203Hg in rabbits additionally exposed to MeHg. A single dose of 203HgCl2 was administered together with or 5 min. or 24 hr after administration of a single dose (10 or 37.5 mumol/kg b.wt.) of MeHg. In another experiment, 203HgCl2 was administered to rabbits subchronically exposed to MeHg (1 mumol/kg b.wt. daily for three weeks) 24 hr after cessation of treatment. The integrity of the blood-brain barrier was assayed by measuring the uptake of 203Hg in the brain, as the blood-brain barrier usually serves to exclude inorganic Hg from the brain. The concentration of 203Hg within the brain was similar in all MeHg-treated rabbits, corresponding to 0.02% of the administered dose, and not different from that of control animals. Under these conditions, no obvious damage to the blood-brain barrier by MeHg could be observed.
先前的研究表明,高剂量接触汞化合物会改变实验动物血脑屏障的完整性和功能。在本研究中,我们研究了静脉注射无机203Hg在额外接触甲基汞的兔子体内的分布情况。单次剂量的203HgCl2与单次剂量(10或37.5 μmol/kg体重)的甲基汞同时给药,或在给药后5分钟或24小时给药。在另一项实验中,在停止治疗24小时后,将203HgCl2给予亚慢性接触甲基汞(每天1 μmol/kg体重,持续三周)的兔子。通过测量脑中203Hg的摄取来测定血脑屏障的完整性,因为血脑屏障通常可阻止无机汞进入大脑。所有接受甲基汞治疗的兔子脑中203Hg的浓度相似,相当于给药剂量的0.02%,与对照动物无差异。在这些条件下,未观察到甲基汞对血脑屏障有明显损害。