4.7 Article

Perinatal exposure to low doses of cypermethrin induce the puberty-related hormones and decrease the time to puberty in the female offspring

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 2, Pages 2665-2675

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-022-22328-x

Keywords

Pyrethroids; Cypermethrin; Pubertal onset; HPG axis; Female offspring

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This study found that perinatal exposure to low doses of cypermethrin (CP) can promote the onset of puberty and regulate puberty-related hormones through the hypothalamic-pituitary-ovarian axis.
Pyrethroid insecticides are ubiquitously detected in environmental media, food, and urine samples. Our previous epidemiological study reported a correlation between increased pyrethroid exposure and delayed pubertal development in Chinese girls. In this study, we further investigated the effects of perinatal exposure to low doses of cypermethrin (CP) on pubertal onset and hypothalamic-pituitary-ovarian axis in the female mice offspring. The treatment of CP with 60 mu g/kg/day from gestation day 6 (GD6) to postnatal day 21 (PND21) significantly decreased the time to puberty in the female offspring. Exposure of CP increased the serum levels of gonadotropin-releasing hormone (GnRH) and the expression of GnRH genes in a dose-dependent manner in the female offspring. CP also induced the serum levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as the expression of gonadotropin subunit genes [LH beta, FSH beta, and chorionic gonadotropin alpha (Cg alpha)]. Furthermore, CP induced serum estradiol (E-2) levels and the expression of steroidogenesis-related genes [steroidogenic acute regulatory (StAR) and Cytochrome p 450, family 11, subfamily A, polypeptide 1 (CYP11A1)] in the ovary. In accordance with the in vivo tests, administration of CP (6.7, 20, and 60 mu g/L) stimulated a dose-dependent increase in the synthesis and secretion of the puberty-related hormones in the explants of hypothalamus, pituitary, and ovary. The interference with calcium channels in the ovary may be responsible for CP-induced pubertal onset. Our study provided evidence that perinatal exposure to low doses of CP induced puberty-related hormones and decreased the time to puberty in the female offspring.

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