Gholami, Mohammadreza and Nemati, Afsaneh and Alasvand Zarasvand, Azita and Zendehdel, Abolfazl and Jalili, Cyrus and Rashidi, Iraj and Mansouri, Kamran and Taheri, Forough and Assadollahi, Vahideh and Gholami, Elham (2024) Selenium mitigates methotrexate-induced testicular injury: Insights from male NMRI mice model. Birth defects research.
Full text not available from this repository.Abstract
Background and aim: Chemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX-induced testicular injury. Materials and methods: Male mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) levels. Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p < .05). Results: Histopathological analysis revealed significant testicular damage in the MTX group, with decreased spermatogenesis and Leydig cell count, while Se administration mitigated these effects, preserving the structural integrity of the reproductive epithelium. Biochemical analysis demonstrated that MTX led to elevated malondialdehyde (MDA) levels and reduced testosterone, LH, and FSH levels, suggesting oxidative stress and Leydig cell dysfunction. Gene expression analysis indicated that MTX upregulated proapoptotic genes (casp3, p53, and bax) while downregulating the antiapoptotic Bcl2 gene. In contrast, Se treatment reversed these trends, highlighting its potential antiapoptotic properties. Conclusion: Our findings underscore the potential of Se as a therapeutic agent to mitigate the reproductive toxicity associated with MTX-induced testicular injury. Se exerts protective effects by regulating oxidative stress, preserving hormone balance, and modulating apoptotic pathways. These results suggest that Se supplementation could be a promising strategy to alleviate chemotherapy-induced testicular damage and preserve male fertility. Keywords: apoptosis; male reproduction; methotrexate; oxidative stress; selenium.
| Item Type: | Article |
|---|---|
| Subjects: | R Medicine > R Medicine (General) R Medicine > RC Internal medicine R Medicine > RZ Other systems of medicine |
| Divisions: | Faculty of Medicine, Health and Life Sciences > School of Medicine |
| Depositing User: | samira sepahvandy |
| Date Deposited: | 17 Feb 2024 08:34 |
| Last Modified: | 17 Feb 2024 08:34 |
| URI: | http://eprints.lums.ac.ir/id/eprint/4684 |
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