Maternal cypermethrin exposure during lactation impairs testicular development and spermatogenesis in male mouse offspring.
Within the last decade, numerous epidemiological studies have demonstrated that endocrine disruptors are a possible cause for a decline in semen quality. Cypermethrin is a widely used pyrethroid insecticide, but little is known about its potentially adverse effects on male reproduction. In the present study, we investigated the effects of maternal cypermethrin exposure during lactation on testicular development and spermatogenesis in male offspring. Maternal mice were administered with cypermethrin (25 mg/kg) by gavage daily from postnatal day 0 (PND0) to PND21. Results showed that the weight of testes at PND21 was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Maternal cypermethrin exposure during lactation markedly decreased the layers of spermatogenic cells, increased the inside diameter of seminiferous tubules, and disturbed the array of spermatogenic cells in testes of pups at PND21. In addition, maternal cypermethrin exposure during lactation markedly reduced mRNA and protein levels of testicular P450scc, a testosterone (T) synthetic enzyme. Correspondingly, the level of serum and testicular T at weaning was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Although the expression of testicular T synthetic enzymes and serum and testicular T in adulthood had restored to control level, the decreased testicular weight and histological changes were irreversible. Importantly, the number of spermatozoa was significantly decreased in adult male offspring whose mothers were exposed to cypermethrin during lactation. In conclusion, maternal cypermethrin exposure during lactation permanently impairs testicular development and spermatogenesis in male offspring, whereas cypermethrin-induced endocrine disruption is reversible.
Wang
Hua
H
Department of Toxicology, Anhui Medical University, Hefei 230032, China.
Wang
Su-Fang
SF
Ning
Huan
H
Ji
Yan-Li
YL
Zhang
Cheng
C
Zhang
Ying
Y
Yu
Tao
T
Ma
Xing-Hao
XH
Zhao
Xian-Feng
XF
Wang
Qun
Q
Liu
Ping
P
Meng
Xiu-Hong
XH
Xu
De-Xiang
DX
D015067:17-Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D000818:Animals; D002786:Cholesterol Side-Chain Cleavage Enzyme / Q000235:genetics / Q000378:metabolism; D052244:Endocrine Disruptors / Q000633:toxicity*; D005260:Female; D005298:Fertility / Q000187:drug effects; D006913:Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D007306:Insecticides / Q000633:toxicity; D007774:Lactation; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D051379:Mice; D008813:Mice, Inbred ICR; D009929:Organ Size / Q000187:drug effects; D011722:Pyrethrins / Q000633:toxicity*; D055101:Semen Analysis; D013076:Sperm Count; D013091:Spermatogenesis / Q000187:drug effects*; D013094:Spermatozoa / Q000187:drug effects / Q000378:metabolism; D013737:Testis / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013739:Testosterone / Q000097:blood / Q000378:metabolism
D052244:Endocrine Disruptors; D007306:Insecticides; D011722:Pyrethrins; C017160:cypermethrin; D013739:Testosterone; D015067:17-Hydroxysteroid Dehydrogenases; D006913:Hydroxysteroid Dehydrogenases; C035507:3(17)-hydroxysteroid dehydrogenase; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D002786:Cholesterol Side-Chain Cleavage Enzyme