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dc.contributor.authorQiu, L.
dc.contributor.authorChen, M.
dc.contributor.authorWang, X.
dc.date.accessioned2019-06-05T18:28:18Z
dc.date.available2019-06-05T18:28:18Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85049152275&doi=10.1093%2fTOXSCI%2fKFX261&partnerID=40&md5=8df463b392dc2e75a2c63d36e845fe63
dc.identifier.urihttp://hdl.handle.net/10713/9445
dc.description.abstractEpidemiological studies link ambient fine particulate matter (PM2.5) pollution to abnormalities in the male reproductive system. However, few toxicological studies have investigated this potentially important adverse effect of PM2.5 pollution. Therefore, in the present study, we analyzed the effects of PM2.5 exposure on spermatogenesis and hypothalamic-pituitary-gonadal (HPG) axis in a murine model. Fourteen male C57BL/6J mice were subjected to a 4-month exposure to filtered air or concentrated ambient PM2.5 (CAP). Their sperm count, testicular histology, spermatogenic parameters, and the major components of HPG axis were assessed. Exposure to CAP significantly reduced sperm count in the epididymis. This was accompanied by Sertoli cell vacuolization, immature germ cell dislocation, and decreases in pachytene spermatocytes and round spermatids of stage VII seminiferous tubules, suggesting a marked impairment of spermatogenesis in these mice. This impairment of spermatogenesis appeared to be attributable to a suppression of HPG axis subsequent to CAP exposure-induced hypothalamic inflammation, as exposure to CAP significantly increased TNFα and IL1b mRNA levels and meanwhile decreased gonadotropin-releasing hormone mRNA expression in the hypothalamus. Moreover, CAP exposure significantly reduced circulating testosterone and follicle-stimulating hormone, testicular testosterone and mRNA expression of follicle-stimulating hormone target gene SHBG and luteinizing hormone target genes P450scc, 17βHSD, and StAR. The present data demonstrate that exposure to ambient PM2.5 impairs spermatogenesis in murine model, raising the concern over effects of ambient PM2.5 pollution on the male reproductive function. Copyright The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.en_US
dc.description.sponsorshipScience Foundation of China (Grant No. 81302452 to L.Q., 81270342 to Z.Y., 81500216 to M.C., 21407082 to X.W.), and Scientific Research Starting Foundation for The Doctoral Researcher of Nantong University (No. 14B14).en_US
dc.description.urihttps://dx.doi.org/10.1093/TOXSCI/KFX261en_US
dc.language.isoen-USen_US
dc.publisherOxford University Pressen_US
dc.relation.ispartofToxicological Sciences
dc.subjectAmbient fine particulate matter (PM 2.5 )en_US
dc.subjectHypothalamic-pituitary-gonadal axisen_US
dc.subjectInflammationen_US
dc.subjectMale reproductive systemen_US
dc.subjectSpermatogenesisen_US
dc.titleExposure to concentrated ambient PM 2.5 compromises spermatogenesis in a mouse model: Role of suppression of hypothalamus-pituitary-gonads axisen_US
dc.typeArticleen_US
dc.identifier.doi10.1093/TOXSCI/KFX261
dc.identifier.pmid29165613


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