Prenatal exposure to diesel exhaust particles and effect on the male reproductive system in mice

Tidsskriftartikel - 2009

Resume

In utero exposure to diesel exhaust particles may reduce sperm production in adulthood. We investigated the effect of prenatal exposure to diesel exhaust particles on the male reproductive system and assessed endocrine disruption and regulation of aquaporin expression as possible mechanisms of action. Dams inhaled 20 mg/m3 of diesel exhaust particle standard reference material 2975 (SRM2975) or clean air for 1 h/day on day 7-19 during pregnancy. Male offspring were killed on day 170 after birth. The dams that had inhaled SRM2975 delivered offspring, which in adulthood had reduced daily sperm production (P = 0.046, Mann-Whitney U-test), whereas there were no differences in the body weight, testis weight and anogenital distance. There was no difference in plasma testosterone and estradiol concentrations, although some samples were not analyzed precisely because of technical problems. The gene regulation of the androgen receptor, anti-Müllerian hormone, estrogen receptor-a, estrogen receptor-ß, follicle-stimulating hormone receptor, insulin-like growth factor 3, luteinising hormone receptor, and aromatase in testes, were not significantly altered in the group exposed in utero to SRM2975 compared to controls. These data indicate that prenatal exposure to SRM2975 was not associated with endocrine disruptor activity in adulthood. There was no significant change in expression levels of aquaporins 7, 8 and 9 in testes tissue, measured as mRNA expression and protein levels by immunohistochemistry. In conclusion, prenatal exposure to SRM2975 was associated with reduced daily sperm production in adulthood, which was not possible to clearly associate with altered endocrine function or expression of aquaporins in the testes.

Reference

Hemmingsen J, Hougaard KS, Talsness C, Wellejus A, Loft S, Wallin EHR, Møller P. Prenatal exposure to diesel exhaust particles and effect on the male reproductive system in mice. Toxicology 2009;264(1-2):61-68.
doi: 10.1016/j.tox.2009.07.012

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