Ciprofloxacin and enrofloxacin can cause reproductive toxicity via endocrine signaling pathways.
In: Ecotoxicology & Environmental Safety, Jg. 244 (2022-10-01), S. N.PAG
Online
academicJournal
Zugriff:
Ciprofloxacin (CIP) and enrofloxacin (ENR) are veterinary antibiotics commonly utilized to treat and prevent animal diseases. Environmental and dietary antibiotic residues can directly and indirectly affect the reproductive development of animals and humans. This article investigated the reproductive toxicity of CIP in male zebrafish, showing that it could decrease the spermatogonial weight and damage the spermatogonial tissue. The sex hormone assays showed that CIP decreased fshb and lhb gene expression and plasma testosterone (T). In addition, transcriptome analysis indicated that the effect of CIP on zebrafish might be related to the endocrine signaling pathways. ENR, which was selected for further study, inhibited mouse Leydig (TM3) and Sertoli (TM4) cell proliferation and caused cell cycle arrest. The sperm concentration, serum luteotropic hormone (LH) and follicle-stimulating hormone (FSH), and T levels decreased in adolescent mice after ENR treatment for 30d in vivo. Hematoxylin and eosin (H&E) staining showed that ENR exposure potentially induced testicular injury, while the real-time quantitative PCR (qPCR) results indicated that ENR inhibited the mRNA expression of key genes in the Leydig cells (cyp11a1, 3β-HSD, and 17β-HSD), Sertoli cells (Inhbβ and Gdnf) and spermatogenic cells (Plzf, Stra8 and Dmc1). In conclusion, these findings indicated that ENR exposure might influence the development of the testes of pubescent mice. [Display omitted] • Fluoroquinolone antimicrobials can damage the reproductive system in males. • CIP can damage the reproductive system of male zebrafish. • ENR affects the viability and inhibits cell cycle progress in TM3 and TM4 cells. • Puberty mice ENR exposure reduces hormone levels and delays testicular development. [ABSTRACT FROM AUTHOR]
Titel: |
Ciprofloxacin and enrofloxacin can cause reproductive toxicity via endocrine signaling pathways.
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Autor/in / Beteiligte Person: | Hou, Lirui ; Fu, Yuhan ; Zhao, Chong ; Fan, Lihong ; Hu, Hongbo ; Yin, Shutao |
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Zeitschrift: | Ecotoxicology & Environmental Safety, Jg. 244 (2022-10-01), S. N.PAG |
Veröffentlichung: | 2022 |
Medientyp: | academicJournal |
ISSN: | 0147-6513 (print) |
DOI: | 10.1016/j.ecoenv.2022.114049 |
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