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• W2158886103 abstract "Disorders of the male reproductive system are increasing in prevalence. The term testicular dysgenesis syndrome emphasizes the importance of developmental influences on the aetiology of conditions including cryptorchidism, testicular germ cell cancer and reduced spermatogenesis. Men whose mothers smoked during pregnancy have lower sperm production. Cigarette smoke contains agents acting on the aryl hydrocarbon receptor (AHR). We have investigated the presence of AHR in the developing human testis and the effects of functional activation.Immunohistochemistry determined AHR to be expressed by germ cells in the human testis between 7 and 19 week gestation, but not by other cells. Treatment of cultured fetal testis with an AHR ligand present in tobacco smoke increased markers of cell apoptosis, and this was prevented by an AHR receptor antagonist. Immunohistochemistry indicated that apoptosis was restricted to germ cells.Germ cells in the developing human testis are a target for regulation by AHR ligands. Activation of AHR by environmental toxicants and AHR-induced apoptotic pathways may be the mechanism of action underlying the epidemiological findings of reduced spermatogenesis in men exposed to cigarette smoke before birth, and may also be of importance in other conditions comprising the testicular dysgenesis syndrome." @default.
• W2158886103 created "2016-06-24" @default.
• W2158886103 creator A5009663084 @default.
• W2158886103 creator A5028516152 @default.
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• W2158886103 date "2007-09-27" @default.
• W2158886103 modified "2023-10-16" @default.
• W2158886103 title "Environmental toxicant-induced germ cell apoptosis in the human fetal testis" @default.
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• W2158886103 doi "https://doi.org/10.1093/humrep/dem300" @default.
• W2158886103 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17890726" @default.
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