Genetic variation in susceptibility to endocrine disruption by estrogen in mice
Genetic variation in susceptibility to endocrine disruption by estrogen in mice
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DOI：
10.1126/science.285.5431.1259
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发表时间：
1999-08-20
期刊：
影响因子：
56.9
通讯作者：
Barkley, M
中科院分区：
文献类型：
--
作者：
Spearow, JL;Doemeny, P;Barkley, M
不同品系小鼠对17 β-雌二醇（E-2）破坏幼年雄性生殖发育的敏感性存在较大差异（超过16倍）。品系、E-2剂量以及品系与E-2剂量的交互作用对睾丸重量和精子发生的影响均达到极显著水平（P < 0.0001）。在C57 BL/6 J和C17/J1 s等品系中，低剂量E-2可消除精细胞成熟。与此相反，广泛使用的CD-1系小鼠，这已被选定为大的产仔数，表现出很少或没有抑制精子细胞成熟，即使在响应16倍多的E-2。对选择的繁殖力动物进行的产品安全性生物测定可能大大低估了雌二醇和环境雌激素化合物对雄性生殖发育的破坏。
Large (more than 16-fold) differences in susceptibility to disruption of juvenile male reproductive development by 17 beta-estradiol (E-2) were detected between strains of mice. Effects of strain, E-2 dose, and the interaction of strain and E-2 dose on testes weight and spermatogenesis were all highly significant (P < 0.0001). Spermatid maturation was eliminated by low doses of E-2 in strains such as C57BL/6J and C17/Jls. In contrast, mice of the widely used CD-1 line, which has been selected for large litter size, showed Little or no inhibition of spermatid maturation even in response to 16 times as much E-2. Product safety bioassays conducted with animals selected for fecundity may greatly underestimate disruption of male reproductive development by estradiol and environmental estrogenic compounds.