Selenium mitigates methotrexate-induced testicular injury: Insights from male NMRI mice model.

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.

Osteogenic effect of electromagnetic fields on stem cells derived from rat bone marrow cultured in osteogenic medium versus conditioned medium in vitro.

OBJECTIVES: This study assessed possible osteogenic differentiation caused by electromagnetic fields (EMF) on rat bone-marrow-derived stem cells (rBMSCs) cultured in osteogenic medium (OM) or in human adipose-stem cell-conditioned medium (hADSC-CM). MATERIALS AND METHODS: The rBMSCs were divided into negative and positive control groups, cultured in α-MEM plus 10% FBS or OM respectively. CM and CM + EMF  groups, cultured cells in hADSCs-CM or exposed to EMF (50 Hz, 1 mT) for 30 min/day plus hADSCs-CM, respectively. Cells from the OM + EMF were simultaneously cultured in OM and exposed to EMF. Osteogenesis was investigated through alkaline phosphatase activity, alizarin red staining and real-time PCR. RESULTS: A meaningfully higher level of ALP activity was observed in the OM + EMF group compared to the other groups. There was a considerable increase in Runx2 expression in the CM + EMF group compared to the positive control and CM groups and a significant increase in Runx2 expression in the OM + EMF in comparison with all other groups after 21 days. Runx2 expression increased significantly in the CM, CM + EMF and positive control groups on day 21 compared to the same groups on day 14. From days 14-21, Ocn expression increased in the CM and CM + EMF groups, but both groups showed a significant decrease compared to the positive controls. CM and EMF had no effect on Ocn expression. On day 21, Ocn expression was significantly higher in the OM + EMF group than in the positive control group. CONCLUSION: The synergistic effect of EMF and OM increased the expression of Runx2 and Ocn in rBMSCs.