caa a22 4500 445852860 CHVBK 20180317145418.0 cr unu---uuuuu 170323e20110901xx s 000 0 eng 10.1007/s00204-011-0654-9 doi (NATIONALLICENCE)springer-10.1007/s00204-011-0654-9 Fenvalerate induces germ cell apoptosis in mouse testes through the Fas/FasL signaling pathway [Elektronische Daten] [Xian-Feng Zhao, Qun Wang, Yan-Li Ji, Hua Wang, Ping Liu, Cheng Zhang, Ying Zhang, De-Xiang Xu] Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with fenvalerate (15 or 60mg/kg) by gavage for 28days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII-VIII and also stages IX-XII seminiferous tubules in testes. Additional experiments showed that fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway. Springer-Verlag, 2011 Fenvalerate nationallicence Testis nationallicence Germ cells nationallicence Apoptosis nationallicence Fas/FasL pathway nationallicence Zhao Xian-Feng Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Wang Qun Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Ji Yan-Li Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Wang Hua Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Liu Ping Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Zhang Cheng Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Zhang Ying Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Xu De-Xiang Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut Archives of Toxicology Springer-Verlag 85/9(2011-09-01), 1101-1108 0340-5761 85:9<1101 2011 85 204 https://doi.org/10.1007/s00204-011-0654-9 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00204-011-0654-9 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Zhao Xian-Feng Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Wang Qun Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Ji Yan-Li Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Wang Hua Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Liu Ping Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Zhang Cheng Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Zhang Ying Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 700 1- Xu De-Xiang Department of Toxicology, Anhui Medical University, 230032, Hefei, China aut NATIONALLICENCE 773 0- Archives of Toxicology Springer-Verlag 85/9(2011-09-01), 1101-1108 0340-5761 85:9<1101 2011 85 204 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer