Recurrent Exposure to Amoxicillin Impairs Male Reproductive Function by Enhancing Oxidative Stress and DNA Fragmentation in the Testis of Swiss Albino Mice
The present study was designed to investigate the impact of recurrent exposure to amoxicillin on the male reproductive system by employing a multi-parametric approach in a mouse model. Animals (n = 20) were randomly assigned into two groups: Group I served as a negative control while Group II was treated with amoxicillin every alternative week for 10 weeks. At the end of the experiment period, five animals (n = 05) from each group were euthanised, blood and tissue samples were utilised for further analysis, and the remaining five (n = 05) animals per group were utilised to assess the fertility index. Ultrastructural and sperm parameter analyses and histomorphology assessment of the testis revealed significant impairments (p < 0.05) following amoxicillin exposure. Amoxicillin exposure also caused significant elevation of oxidative stress and double strand DNA breaks in testicular cells as demonstrated by increased level of 8-OHdG and γ-H2AX positive cells in the testis (p < 0.001). To summarise, this study indicated that recurrent exposure to amoxicillin can induce reproductive toxicity through oxidative stress and genotoxic mechanisms, compromising sperm integrity and fertility potential in male mice. This work highlights the need for evaluation of antibiotic safety concerning male reproductive health, with implications for clinical practice, environmental exposures and the development of strategies to mitigate fertility risks.
Authors
- Samir Thakur
- Manuj Kr. Bharali (ORCID: https://orcid.org/0000-0002-3939-5930)
- Mrinmoy Chakraborty (ORCID: https://orcid.org/0000-0003-2843-3142)
- Nabila Akhtara
Institutions
- Gauhati University (IN)
Publication Details
- Journal
- Basic & Clinical Pharmacology & Toxicology
- Published
- 2025-09-16
- DOI
- https://doi.org/10.1111/bcpt.70115
- Primary Topic
- Sperm and Testicular Function
- Type
- article
- Field-Weighted Citation Impact
- 0.00