DEMETHYLATION OF METHYL MERCURY IN DIFFERENT BRAIN SITES OF MACACA-FASCICULARIS MONKEYS DURING LONG-TERM SUBCLINICAL METHYL MERCURY EXPOSURE
DEMETHYLATION OF METHYL MERCURY IN DIFFERENT BRAIN SITES OF MACACA-FASCICULARIS MONKEYS DURING LONG-TERM SUBCLINICAL METHYL MERCURY EXPOSURE
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DOI：
10.1006/taap.1995.1193
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发表时间：
1995-10-01
影响因子：
3.8
通讯作者：
BURBACHER, TM
中科院分区：
文献类型：
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作者：
VAHTER, ME;MOTTET, NK;BURBACHER, TM
测定了甲基汞(MeHg)每日口服剂量(50微克汞/千克体重)或持续静脉注射氯化汞(200微克汞/千克体重)6、12或18个月后，雌性短尾猴大脑特定部位(小脑、枕极、围栏、运动带、额极、颞极、丘脑和垂体)的总汞(T-Hg)和无机汞(I-Hg)浓度。在正常体重(2.4-4.1千克体重)的猕猴中，除6个月时脑下垂体为3.0微克汞/克，12个月时为4.2微克/克，18个月时为4.3微克汞/克外，其余脑部的平均甲基汞浓度(T-汞减去i-汞)大致相同。脑下垂体中的甲基汞浓度约为大脑其他部位的50%。在一组猴子中，在12个月的甲基汞暴露后6个月没有接触甲基汞，除了脑下垂体外，所有大脑部位的甲基汞的T1/2大约是37天。随着甲基汞暴露时间的延长，各脑区的i-Hg浓度均呈上升趋势，尤以丘脑和脑垂体区最为明显。在大多数脑部位，6个月和12个月时I-Hg约占T-Hg的9%，18个月时约占T-Hg的12%。在垂体中，I-Hg从6个月时T-Hg的20%增加到18月时的46%。I-汞的消除T1/2时间非常长，在大多数脑部位为230-540天，在丘脑和脑垂体的消除时间则相当长。在清除期间(6个月)，丘脑中的i-汞浓度没有下降，而垂体中的i-汞浓度在没有额外暴露的情况下继续增加。与接触氯化汞的猴子相比，接触甲基汞的猴子大脑中的i-汞浓度高出数倍，这表明i-汞是通过大脑中甲基汞的去甲基化形成的，而不是通过大脑摄取身体其他部位去甲基化形成的i-汞而形成的。不同个体之间的i-Hg相对浓度有很大差异，但不同大脑部位(丘脑和脑下垂体除外)之间的相对浓度差异不大。暴露于甲基汞的肥胖猴子(体重5.0-6.1千克)在除脑下垂体外的所有大脑部位的甲基汞和异丙基汞的浓度都高于正常体重的猴子。(C)1995年学术出版社。
Total (T-Hg) and inorganic (I-Hg) mercury concentrations were determined in specific brain sites (cerebellum, occipital pole, pens, motor strip, frontal pole, temporal pole, thalamus, and pituitary) of female Macaca fascicularis monkeys exposed to daily peroral doses (50 mu g Hg/kg body weight) of methyl mercury (MeHg) for 6, 12, or 18 months, or to continuous iv infusion of HgCl2 (200 mu g Hg/kg body wt). In normal weight monkeys (2.4-4.1 kg body wt), the average concentration of MeHg (calculated as T-Hg minus I-Hg) was about the same in all brain sites, except the pituitary-3.0 mu g Hg/g at 6 months, 4.2 mu g/g at 12 months, and 4.3 mu g Hg/g at 18 months. MeHg concentrations in the pituitary were about 50% of those in the other brain sites. In a group of monkeys that were kept unexposed for 6 months following 12 months of MeHg exposure, T1/2 for MeHg was about 37 days in all brain sites, with the exception of the pituitary, where it was shorter. The concentration of I-Hg increased in all brain sites, but especially in the thalamus and pituitary, with the time of MeHg exposure. In most brain sites, I-Hg constituted about 9% of T-Hg at 6 and 12 months, and 12% of T-Hg at 18 months. In the pituitary, I-Hg increased from 20% of T-Hg at 6 months to 46% at 18 months. Elimination T1/2 for I-Hg was extremely long, 230-540 days in most brain sites and considerably longer in the thalamus and pituitary. The concentration of I-Hg in the thalamus did not decrease during the clearance period (6 months), while I-Hg in the pituitary continued to increase in spite of no additional exposure. The MeHg exposed monkeys had several times higher I-Hg concentrations in the brain than monkeys exposed to HgCl2, indicating that I-Hg was formed by demethylation of MeHg in the brain, and not by brain uptake of I-Hg formed by demethylation elsewhere in the body. There were large variations in the relative concentration of I-Hg between individual monkeys, but not between brain sites (except thalamus and pituitary). Obese monkeys (5.0-6.1 kg body wt) exposed to MeHg had higher concentrations of both MeHg and I-Hg than normal weight monkeys in all brain sites, except in the pituitary. (C) 1995 Academic Press, Inc.