Evaluation of the effects of deltamethrin on the fetal rat testis

Pyrethroids are among the most commonly used classes of insecticides worldwide. Human exposure to pyrethroids is widespread, as evidenced by the presence of their metabolites in urine of adults, children, and pregnant and lactating women among the general population of several countries. Residues in food and dust, residential outdoor and indoor pesticide applications, and impregnated fabric are potent dermal, inhalation, and oral sources of exposure. Studies in adults and pubescent rats and mice suggest that some of pyrethroids such as deltamethrine, may affect the male reproductive system and may have endocrine disrupting effects involving testosterone biosynthesis. Less is known about the reproductive effects of gestational pyrethroids exposure on male offspring. The purpose of this experimental study is to address whether prenatal exposure to deltamethrin affects the development of the testes in rat fetuses. We more specifically focused on testosterone biosynthetic pathway, since testosterone is essential in normal testicular development.
Sprague-Dawley rats were administered deltamethrin (>98 % pure) at doses ranging from 0.1 to 10 mg/kg/day or 250 mg/kg/day of di-n-hexyl phthalate (DnHP, positive reference) by gavage, on gestational day (GD) 13 to GD 19, which covers the male sexual differentiation period. Both testes were isolated from GD 19 fetuses (three or four fetuses per litter, four litters per group) and were submitted to quantitative real time PCR or Western blot. Our data confirm that DnHP reduces fetal testicular expression of Star and Cyp 11 a (gene and proteins), which are involved in steroid synthesis. No significant changes were observed after prenatal exposure to deltamethrin up to maternal toxic doses. In addition, deltamethrin-exposed male fetuses did not show significant decrease in the anogenital distance, a sensitive marker of antiandrogenic activity.