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We investigated the effects and possible mechanism of action of BPS on adult male C57BL\/6 mice. We found that exposure to 200\u2010mg\/kg BPS resulted in a significant decrease in the sperm count in the caput\/corpus and cauda epididymis, significantly decreased sperm motility, and significantly increased the sperm deformity. Histological evaluation revealed that BPS exposure caused a decrease of spermatozoa in the lumen of seminiferous tubules and a reduction in the proportion of Stage VII or VIII seminiferous tubules in the BPS\u2010treated groups. Furthermore, ultrastructure analysis revealed BPS\u2010induced mitochondrial damage and apoptosis in spermatogenic cells. Moreover, BPS exposure\u2010induced oxidative stress in testicular tissues. Further, dUTP\u2010biotin nick end labeling (TUNEL) assay showed that BPS induced the apoptosis of spermatogenic cells in a dose\u2010dependent manner. BPS also significantly upregulated cleaved caspase\u20108, cleaved caspase\u20109, cleaved caspase\u20103, Fas, and FasL and significantly downregulated the Bcl\u20102\/Bax ratio. These results suggest that BPS\u2010induced oxidative stress in the testis and spermatogenic cell apoptosis potentially impairs spermatogenesis and sperm function, which may be the mechanism of the reproductive toxicity of BPS. The Fas\/FasL and mitochondrial signal pathways may be involved in BPS\u2010induced oxidative stress\u2010related apoptosis. These results suggest that BPS\u2010induced oxidative stress in the testis and spermatogenic cell apoptosis potentially impairs spermatogenesis and sperm function, which may be the mechanism of the reproductive toxicity of BPS. The Fas\/FasL and mitochondrial signal pathways may be involved in BPS\u2010induced oxidative stress\u2010related apoptosis.<\/jats:p>","DOI":"10.1002\/jat.4170","type":"journal-article","created":{"date-parts":[[2021,5,17]],"date-time":"2021-05-17T21:22:21Z","timestamp":1621286541000},"page":"1839-1851","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Oxidative stress\u2010mediated apoptosis is involved in bisphenol S\u2010induced reproductive toxicity in male C57BL\/6 mice"],"prefix":"10.1002","volume":"41","author":[{"given":"Wei","family":"Dai","sequence":"first","affiliation":[{"name":"Department of Preventive Medicine University of South China  Hengyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing\u2010zhi","family":"He","sequence":"additional","affiliation":[{"name":"Department of Occupational and Environmental Health Guilin Medical University  Guilin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bi\u2010qi","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine University of South China  Hengyang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huai\u2010cai","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine University of South China  Hengyang China"},{"name":"Department of Occupational and Environmental Health Guilin Medical University  Guilin China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,5,17]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1515\/reveh-2019-0034"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/ptr.5385"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.chemosphere.2017.12.118"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.envres.2015.11.029"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrurol.2017.69"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.scitotenv.2017.05.171"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/tox.22696"},{"key":"e_1_2_9_9_1","doi-asserted-by":"publisher","DOI":"10.1093\/molehr\/gay017"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1021\/acs.est.5b05387"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.reprotox.2011.03.003"},{"key":"e_1_2_9_12_1","doi-asserted-by":"publisher","DOI":"10.1021\/tx700366x"},{"key":"e_1_2_9_13_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1110358108"},{"key":"e_1_2_9_14_1","doi-asserted-by":"publisher","DOI":"10.1155\/2016\/1203285"},{"key":"e_1_2_9_15_1","doi-asserted-by":"publisher","DOI":"10.1007\/s11356-019-06553-5"},{"key":"e_1_2_9_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.fertnstert.2014.11.005"},{"key":"e_1_2_9_17_1","doi-asserted-by":"publisher","DOI":"10.1262\/jrd.2013-097"},{"key":"e_1_2_9_18_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2605.2007.00788.x"},{"key":"e_1_2_9_19_1","doi-asserted-by":"publisher","DOI":"10.1007\/s13105-013-0298-8"},{"key":"e_1_2_9_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.fertnstert.2008.05.070"},{"key":"e_1_2_9_21_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.talanta.2016.01.037"},{"key":"e_1_2_9_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.taap.2014.07.025"},{"key":"e_1_2_9_23_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0193387"},{"key":"e_1_2_9_24_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tox.2003.07.003"},{"key":"e_1_2_9_25_1","doi-asserted-by":"publisher","DOI":"10.1002\/ar.22641"},{"key":"e_1_2_9_26_1","doi-asserted-by":"publisher","DOI":"10.1021\/es400329t"},{"key":"e_1_2_9_27_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yrtph.2012.01.004"},{"key":"e_1_2_9_28_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.etap.2004.05.009"},{"key":"e_1_2_9_29_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jchromb.2015.10.041"},{"issue":"9","key":"e_1_2_9_30_1","first-page":"869","article-title":"Programmed cell death: Molecular mechanisms and detection. 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