title: Lactational fenvalerate exposure permanently impairs testicular development and spermatogenesis in mice.
abstract: Fenvalerate, a widely used synthetic pyrethroid insecticide, has been associated with poor semen quality in human being. However, little is known about the effects of lactational fenvalerate exposure on testicular development and spermatogenesis. The purpose of the present study was to investigate the effects of maternal fenvalerate exposure during lactation on testicular development and spermatogenesis in male offspring. Maternal mice were administered with fenvalerate (60 mg/kg) by gavage daily from postnatal day (PND) 0 to PND21. Lactational fenvalerate exposure markedly decreased the absolute and relative weights of testes and increased the number of apoptotic cells in testes of pups at weaning. Histological examinations showed abnormal seminiferous tubules with large vacuoles or complete spermatogenic failure in testes of fenvalerate-treated mice at weaning. Additional experiment showed that lactational fenvalerate exposure markedly reduced mRNA and protein levels of testicular P450scc, a testosterone (T) synthesis enzyme. Consistent with down-regulation of testicular P450scc, the level of serum and testicular T at weaning was significantly decreased in pups whose mothers were exposed to fenvalerate during lactation. Although the expression of testicular P450scc and serum and testicular T in adulthood restored to control level, the decreased weight of testes and histological changes were irreversible. Importantly, the percentage of mature seminiferous tubules (stages VII and VIII) and the number of spermatozoa were obviously decreased in adult male mice whose mothers were exposed to fenvalerate during lactation. Taken together, these results suggest that lactational fenvalerate exposure permanently impairs testicular development and spermatogenesis.
authors.affiliation: Department of Toxicology, Anhui Medical University, Hefei 230032, China.
authors.forename: Heng
authors.initials: H
authors.lastname: Zhang
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.forename: Yan-Li
authors.initials: YL
authors.lastname: Ji
authors.forename: Huan
authors.initials: H
authors.lastname: Ning
authors.forename: Tao
authors.initials: T
authors.lastname: Yu
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xian-Feng
authors.initials: XF
authors.lastname: Zhao
authors.forename: Qun
authors.initials: Q
authors.lastname: Wang
authors.forename: Ping
authors.initials: P
authors.lastname: Liu
authors.forename: Xiu-Hong
authors.initials: XH
authors.lastname: Meng
authors.forename: De-Xiang
authors.initials: DX
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects; D005260:Female; D020567:Fetal Weight / Q000187:drug effects; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007306:Insecticides / Q000633:toxicity*; D007774:Lactation / Q000187:drug effects; D007985:Leydig Cells / Q000187:drug effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009570:Nitriles / Q000633:toxicity*; D009929:Organ Size / Q000187:drug effects; D010750:Phosphoproteins / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011722:Pyrethrins / Q000633:toxicity*; D011863:Radioimmunoassay; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013076:Sperm Count; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000187:drug effects* / Q000201:enzymology / Q000254:growth & development*; D013739:Testosterone / Q000096:biosynthesis / Q000378:metabolism; D000098682:Steroidogenic Acute Regulatory Protein
chemical_list: D007306:Insecticides; D009570:Nitriles; D010750:Phosphoproteins; D011722:Pyrethrins; D000098682:Steroidogenic Acute Regulatory Protein; D013739:Testosterone; C017690:fenvalerate