TOXICOLOGY STUDIES OF LEAD

一项研究比较了铅的毒性和生物利用度。 在暴露于纯铅盐或斯卡格韦铅矿的雄性F344大鼠中， AK.这些化学物质被喂给大鼠30天。在研究终止时领导 血、骨、肾、脑和尿液中的浓度 测定氨基乙酰丙酸。可溶的铅盐、氧化铅和 醋酸铅，在骨骼和软组织中积累的程度比 来自阿肯色州斯卡格韦的不溶性硫化铅或铅矿石。当时有一个 剂量与骨铅浓度之间存在很强的相关性 当数据被绘制在长条上时，可溶或不溶铅样品 线性比例。使用氨基乙酰丙酸生物标志物在以下情况下无效 骨铅浓度低于20微克/克。血铅浓度为~ 饲喂可溶铅盐的大鼠为80mug/dl，饲喂的大鼠为~10mug/dl 硫化铅或铅矿。软组织中铅的最高浓度 发生在肾脏，其次是脑。饲喂可溶性铅盐的大鼠 软组织中积累的铅浓度大约高出10倍 与喂食硫化铅或铅矿石的饲料相比。然而，可检测的和 铅的潜在毒性浓度累积在与剂量相关的 可溶铅含量较低的样品对大鼠肾脏和脑组织的影响； 与饲喂硫化铅的大鼠相比，饲喂铅矿的大鼠的致死率更高。 这些数据表明，较长的暴露时间可能会导致持续的 以及更多的铅积累。大鼠给药后出现肾脏损害 添加30或100ppm的醋酸铅，而不是其他处理组。铅 来自阿拉斯加、密苏里州和科罗拉多州其他三个矿场的矿石样本， 被喂以更长时间(90天)的大鼠来比较 来自不同地理区域的矿石的生物有效性和毒性。 血液中氨基酮丙酸脱水酶活力的测定 铅中毒的敏感和特异的生物标志物及其测定 血液、肾脏和大脑中的铅在30天、60天和90天进行检测 曝光。来自30d样品的数据表明，饲料中的100ppm 阿拉斯加铅矿和密苏里州铅矿这两个样品显著 抑制血液中ALAD酶活性。

A study was conducted to compare the toxicity and bioavailability of lead in male F344 rats exposed to pure lead salts or to lead ore from Skagway, AK. The chemicals were fed to rats for 30 days. At study termination lead concentrations in blood, bone, kidney, and brain, and urinary aminolevulinic acid were measured. The soluble lead salts, lead oxide and lead acetate, accumulated to a greater degree in bone and soft tissues than the insoluble lead sulfide or the lead ore from Skagway, AK. there was a strong correlation between dose and bone lead concentration for either soluble or insoluble lead samples when the data were graphed on a long- linear scale. Use of the aminolevulinic acid biomarker was ineffective at bone lead concentrations below 20 mug/g. Blood lead concentrations were ~ 80 mug/dl in rats fed the soluble lead salts, and ~ 10 mug/dl in rats fed lead sulfide or lead ore. The highest lead concentrations in soft tissue occurred in kidney, followed by brain. Rats fed soluble lead salts accumulated about 10-fold higher lead concentrations in the soft tissues compared to those fed lead sulfide or lead ore. However, detectable and potentially toxic concentrations of lead accumulated in a dose-related fashion in kidney and brain of rats fed the less soluble lead samples, and to a higher degree in rats fed lead ore compared to those fed lead sulfide. These data suggest that longer exposure periods might result in continual and greater accumulations of lead. Kidney lesions occurred in rats dosed with 30 or 100 ppm lead acetate but not in other treatment groups. Lead ore samples from three other mining sites, Alaska, Missouri, and Colorado, are being fed to rats for longer periods (90 days) to compare the bioavailability and toxicity or ores from different geographical areas. Assays of blood ?-aminolevulinic acid dehydratase enzyme activity, a sensitive and specific biomarker for lead toxicity, and determinations of lead in blood, kidney, and brain are being conducted at 30, 60, and 90d exposure. Data from the 30d samples indicate that at 100ppm in the feed two samples, Alaskan lead ore and Missouri lead ore, significantly inhibited blood ALAD enzyme activity.