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首页> 外文期刊>Archives of Toxicology >Lung tumors in mice induced by 'whole-life' inorganic arsenic exposure at human-relevant doses
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Lung tumors in mice induced by 'whole-life' inorganic arsenic exposure at human-relevant doses

机译：在与人有关的剂量下“全寿命”无机砷暴露引起的小鼠肺部肿瘤

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In mice, inorganic arsenic in the drinking water in the parts per million range via the dam during in utero life or with whole-life exposure is a multi-site carcinogen in the offspring. However, human arsenic exposure is typically in the parts per billion (ppb) range. Thus, we studied "whole-life" inorganic arsenic carcinogenesis in mice at levels more relevant to humans. Breeder male and female CD1 mice were exposed to 0, 50, 500 or 5,000 ppb arsenic (as sodium arsenite) in the drinking water for 3 weeks prior to breeding, during pregnancy and lactation, and after weaning (at week 3) groups of male and female offspring (initial n = 40) were exposed for up to 2 years. Tumors were assessed in these offspring. Arsenic exposure had no effect on pregnant dam weights or water consumption, litter size, offspring birthweight or weight at weaning compared to control. In male offspring mice, arsenic exposure increased (p < 0.05) bronchiolo-alveolar tumor (adenoma or carcinoma) incidence at 50-ppb group (51 %) and 500-ppb group (54 %), but not at 5,000-ppb group (28 %) compared to control (22 %). These arsenic-induced bronchiolo-alveolar tumors included increased (p < 0.05) carcinoma at 50-ppb group (27 %) compared to controls (8 %). An increase (p < 0.05) in lung adenoma (25 %) in the 50-ppb group compared to control (11 %) occurred in female offspring. Thus, in CD1 mice whole-life arsenic exposure induced lung tumors at human-relevant doses (i.e., 50 and 500 ppb).
机译：在小鼠中，子宫内或整个生命期间通过大坝通过饮用水中的百万分之几的无机砷是后代中的多部位致癌物。但是，人的砷暴露通常在十亿分之一（ppb）的范围内。因此，我们以与人类更相关的水平研究了小鼠的“全寿命”无机砷致癌作用。在繁殖前，妊娠和哺乳期间以及断奶后（第3周），雄性和雌性CD1雄性和雌性CD1小鼠在饮用水中分别暴露于0、50、500或5,000 ppb砷（作为亚砷酸钠），持续3周。和雌性后代（初始n = 40）暴露了长达2年。在这些后代中评估肿瘤。与对照组相比，砷暴露对孕妇的水坝体重或水消耗，产仔数，后代出生体重或断奶体重没有影响。在雄性后代小鼠中，50-ppb组（51％）和500-ppb组（54％）的砷暴露增加（p <0.05）细支气管-肺泡肿瘤（腺瘤或癌）的发生率，但在5,000-ppb组则没有（ 28％），而对照组（22％）。这些砷诱导的支气管肺泡肿瘤包括与对照组（8％）相比在50 ppb组（27％）的癌变增加（p <0.05）。 50 ppb组的肺腺瘤（25％）与对照组（11％）相比增加了（p <0.05）。因此，在CD1小鼠中，全生命期砷暴露以与人类相关的剂量（即50和500 ppb）诱导肺肿瘤。

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