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TOXICOLOGY STUDIES OF LEAD

TOXICOLOGY STUDIES OF LEAD
铅的毒理学研究
批准号:
3855860
负责人:
M P DIETER
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
进行了一项合同研究项目,以比较毒性和 氧化铅、硫化铅、醋酸铅的生物可利用度 来自阿拉斯加的铅精矿。这些化学物质被喂给大鼠30天 天数,剂量分别为10、30和100ppm。阿司匹林的相对生物利用度 通过测量不同类型的铅材料的 铅在血液和骨骼中的积聚。尿氨基酮丙酸 被确定为铅毒性的一种衡量标准,可以与 铅致人尿中氨基酮丙酸升高的报道 样本。来自醋酸铅和氧化铅的铅在 骨骼中与剂量相关的方式,如峰值浓度为200-30o 100ppm剂量组可达微克/克。一个稳定的, 与剂量相关,但从铅中积累铅的速度要慢得多 硫化物和阿拉斯加铅精矿样本出现在骨骼中,如 最高浓度可达10-15微克/克。有一个 骨铅升高与尿铅升高之间的强相关性 饲喂可溶性醋酸铅和氧化铅大鼠的氨基乙酰丙酸 盐,但在喂食不溶性硫化铅的大鼠中没有相关性, 阿拉斯加铅精矿。患者的尿氨基酮丙酸没有升高。 后一种动物体内的酸,表明骨铅的积累 在抑制标记物之前,浓度为15 pg/g是必需的 铅中毒的酶,氨基酮丙酸脱水酶,将导致 尿氨基酮丙酸排泄过量。入口处的分析 连续的血液样本,以及组织病理学的评估 骨骼、肾脏、肝脏和大脑都在进行中。此外,还提供了 选定的目标器官从研究中存档,以备将来使用 铅中毒的调查。
英文摘要
A contract research project was conducted to compare the toxicity and bioavailability of lead oxide, lead sulfide, lead acetate, and a sample of lead ore concentrate from Alaska. The chemicals were fed to rats for 30 days at doses of 10, 30, and 100 ppm. The comparative bioavailability of the different types of lead materials were evaluated by measuring the accumulation of lead in the blood and bone. Urinary aminolevulinic acid was determined as a measure of lead toxicity that could be compared to lead-induced elevations of aminolevulinic acid reported in human urine samples. Lead from lead acetate and lead oxide accumulated rapidly in a dose-related fashion in the bone, such that peak concentrations of 200-30O micro-g/gm were attained in the 100 ppm dose group. A steady, dose-related, but much slower rate of accumulation of lead from lead sulfide and the Alaskan lead concentrate sample occurred in the bone, such that peak concentrations of 10-15 micro-g/gm were attained. There was a strong correlation between the elevations in bone lead and that of urinary aminolevulinic acid in rats fed the soluble lead acetate and lead oxide salts, but no correlation in rats fed the insoluble lead sulfide and the Alaskan lead concentrate. There was no elevation of urinary aminolevulinic acid in the latter animals, indicating accumulation of bone lead concentrations >15 pg/gm were necessary before inhibition of a marker enzyme for lead toxicity, aminolevulinic acid dehydratase, would result in excess excretion of urinary aminolevulinic acid. Analyses of lead in serial samples of blood, as well as evaluation of histopathology in the bone, kidney, liver, and brain are in progress. In addition, samples of selected target organs were archived from the study for potential future investigations on lead toxicity.
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