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长期暴露于甲基汞后灵长类动物血液和大脑中汞的形态分析。

Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.

作者信息

Vahter M, Mottet N K, Friberg L, Lind B, Shen D D, Burbacher T

机构信息

Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.

出版信息

Toxicol Appl Pharmacol. 1994 Feb;124(2):221-9. doi: 10.1006/taap.1994.1026.

Abstract

Total (T-Hg) and inorganic (I-Hg) mercury in blood and brain of female Macaca fascicularis monkeys, exposed to daily peroral doses of methyl mercury (MeHg; 50 micrograms Hg/kg body wt) for 6, 12, or 18 months, or to continuous iv infusion of HgCl2 (200 micrograms Hg/kg body wt) for 3 months, were determined. In normal weight monkeys (2.4-4.1 kg body wt) exposed to MeHg, steady state of T-Hg in blood (1.1 micrograms Hg/g) was reached in about 4 months. The elimination T1/2 in blood was 26 days. I-Hg constituted 7% of T-Hg in blood. The average concentration of MeHg in occipital pole and thalamus was about 3 micrograms Hg/g at 6 months and 4.5 micrograms Hg/g at 12-18 months. Accumulation in brain seemed to be biphasic. Following termination of 12 months exposure, elimination T1/2 for MeHg in brain was 35 days. I-Hg constituted about 9% of T-Hg in brain at 6-12 months, 18% at 18 months, and 74% at 6 months after termination of exposure. The I-Hg concentrations were somewhat higher in thalamus than in occipital pole. The elimination T1/2 for I-Hg was extremely long, on the order of years. Most likely, the I-Hg was formed by demethylation of MeHg in the brain. In monkeys exposed to HgCl2, blood levels of 0.6 micrograms I-Hg/g gave rise to brain I-Hg levels of about 0.1 micrograms/g only. In three heavy weight monkeys (5.0-6.1 kg body wt) exposed to MeHg, blood Hg increased to about 2 micrograms Hg/g, indicating a limited distribution of MeHg to fat. The Hg concentrations in brain (7-22 micrograms Hg/g) were considerably higher than those in normal weight monkeys, due to the high blood Hg levels in combination with a high brain-to-blood distribution ratio.

摘要

测定了每日经口给予甲基汞(MeHg;50微克汞/千克体重)6个月、12个月或18个月,或连续静脉输注氯化汞(HgCl2;200微克汞/千克体重)3个月的雌性食蟹猴血液和大脑中的总汞(T-Hg)和无机汞(I-Hg)。在暴露于MeHg的正常体重猴子(体重2.4 - 4.1千克)中,血液中T-Hg的稳态(1.1微克汞/克)在约4个月时达到。血液中的消除半衰期为26天。I-Hg占血液中T-Hg的7%。枕叶和丘脑中MeHg的平均浓度在6个月时约为3微克汞/克,在12 - 18个月时为4.5微克汞/克。大脑中的蓄积似乎呈双相性。在12个月暴露结束后,大脑中MeHg的消除半衰期为35天。I-Hg在暴露6 - 12个月时占大脑中T-Hg的约9%,在18个月时占18%,在暴露结束6个月时占74%。丘脑中的I-Hg浓度略高于枕叶。I-Hg的消除半衰期极长,以年为单位。很可能,I-Hg是由大脑中MeHg的去甲基化形成的。在暴露于HgCl2的猴子中,血液中0.6微克I-Hg/克的水平仅导致大脑中I-Hg水平约为0.1微克/克。在三只暴露于MeHg的超重猴子(体重5.0 - 6.1千克)中,血液汞增加到约2微克汞/克,表明MeHg在脂肪中的分布有限。由于高血汞水平与高脑血分布比相结合,大脑中的汞浓度(7 - 22微克汞/克)明显高于正常体重猴子。

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