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Selenium Mitigates Methotrexate-Induced Testicular Injury: Insights From Male Nmri Mice Model Publisher Pubmed



Gholami M1 ; Nemati A2 ; Zarasvand AA3 ; Zendehdel A4 ; Jalili C5 ; Rashidi I6 ; Mansouri K5 ; Taheri F7 ; Assadollahi V8 ; Gholami E1
Authors
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Authors Affiliations
  1. 1. Fertility and Infertility Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran
  2. 2. Student Research Committee, Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  3. 3. Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, Charlotte, NC, United States
  4. 4. Department of Internal Medicine, Ziaeian Hospital, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Medical Technology Research Center, Institute of Health Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran
  6. 6. Department of Anatomical Sciences, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
  7. 7. Department of Physiology, School of medicine, Lorestan University of Medical Sciences, Khorramabad, Iran
  8. 8. Department of Tissue Engineering & Applied Cell Sciences, School of Advanced Technologies, Shahrekord University of Medical Sciences, Shahrekord, Iran

Source: Birth Defects Research Published:2024


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. © 2024 Wiley Periodicals LLC.
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