Ono Naoka, Oshio Shigeru, Niwata Yuichiro, Yoshida Seiichi, Tsukue Naomi, Sugawara Isamu, Takano Hirohisa, Takeda Ken
Department of Hygiene Chemistry, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.
Arch Toxicol. 2008 Nov;82(11):851-9. doi: 10.1007/s00204-008-0302-1. Epub 2008 May 1.
We recently showed that prenatal exposure to diesel exhaust (DE) disrupts spermatogenesis in mouse offspring. This study was undertaken to determine whether filtered DE in which 99.97% of diesel exhaust particles >0.3 microm in diameter were removed affects spermatogenesis in growing mice. After prenatal exposure to filtered DE for 2-16 days postcoitum, we examined daily sperm production (DSP), testicular histology, serum testosterone levels and mRNA expression of hormone synthesis process-related factors. In the filtered DE exposed group, DSP was markedly reduced at 12 weeks compared with the control group; clean air exposed group. Histological examination showed multinucleated giant cells and partial vacuolation in the seminiferous tubules of the exposed group. Testosterone was elevated significantly at 5 weeks. Moreover, luteinizing hormone receptor mRNA at 5 and 12 weeks, 17alpha-hydroxylase/C17-20-lyase and 17beta-hydroxysteroid dehydrogenase mRNAs at 12 weeks were significantly elevated. These results suggest that filtered DE retains its toxic effects on the male reproductive system following prenatal exposure.
我们最近发现，产前暴露于柴油废气（DE）会破坏小鼠后代的精子发生。本研究旨在确定去除了99.97%直径大于0.3微米的柴油废气颗粒的过滤后DE是否会影响生长中小鼠的精子发生。在产前暴露于过滤后DE 2至16天（受孕后）后，我们检测了每日精子生成量（DSP）、睾丸组织学、血清睾酮水平以及激素合成过程相关因子的mRNA表达。在过滤后DE暴露组中，与对照组（清洁空气暴露组）相比，12周时DSP显著降低。组织学检查显示，暴露组的生精小管中有多核巨细胞和部分空泡化。5周时睾酮显著升高。此外，5周和12周时促黄体生成素受体mRNA、12周时17α-羟化酶/C17-20裂解酶和17β-羟类固醇脱氢酶mRNA均显著升高。这些结果表明，产前暴露后，过滤后DE对雄性生殖系统仍具有毒性作用。
