Testicular damage from electromagnetic radiation in rats and evaluation of protective agents

Male infertility has been associated with various environmental, physiological, and genetic factors. In recent years, the widespread use of mobile phones has raised concerns regarding exposure to electromagnetic radiation (EMR). EMR emitted from mobile devices may adversely affect male reproductive function by inducing oxidative stress and impairing spermatogenesis.

This study aimed to evaluate the potential protective effects of vitamin E and N-acetylcysteine (NAC) against EMR-induced testicular damage in rats.

A total of 35 adult male Wistar rats were randomly divided into five groups (n = 7 per group): control, EMR exposure, EMR + NAC, EMR + vitamin E, and EMR + NAC + vitamin E. Rats were exposed to EMR generated by a mobile phone operating in the GSM frequency band (900/1800 MHz) in active call mode, positioned at a fixed distance of 15 cm from the cages, for 3 h daily over 28 days. The specific absorption rate (SAR) was based on manufacturer-reported values. Biochemical analyses were performed to assess total antioxidant capacity (TAC), glutathione peroxidase (GPX), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. Data distribution was evaluated using the Shapiro-Wilk test, and group comparisons were conducted using the Kruskal-Wallis test with appropriate post-hoc analyses.

Significant differences were observed among groups in terms of total antioxidant capacity (TAC) (p < 0.001). TAC levels were reduced in the EMR-only group compared to controls, whereas antioxidant supplementation (NAC and/or vitamin E) resulted in increased TAC levels. Post-hoc analyses demonstrated significant improvements in TAC in treatment groups compared to both control and EMR-only groups. However, no statistically significant differences were observed among groups for GPX, SOD, and MDA levels (p > 0.05).

N-acetylcysteine (NAC) and vitamin E may exert partial protective effects against EMR-induced oxidative alterations in rat testes, particularly as reflected by improvements in total antioxidant capacity. However, given that other oxidative stress markers did not demonstrate statistically significant differences, these findings should be interpreted with caution. Further experimental and clinical studies with larger sample sizes and detailed histopathological evaluation are required to better elucidate the potential therapeutic role and clinical relevance of these antioxidant agents.