The Influence of 2.45 GHz Wi-Fi Exposure Duration on Sperm Quality and Testicular Histopathology: An Exploration of Peroxidative Injury.

Given the ubiquitous use of Wi-Fi technology, it is more urgent than ever to evaluate its potential health implications. One concern is the effect of non-ionizing radiation on the male reproductive system, a topic that has drawn increased scientific and public attention. One potential mechanism through which 2.45 GHz Wi-Fi radiation may cause harm is by inducing oxidative stress. A common biomarker of oxidative stress is malondialdehyde (MDA), a by-product of lipid peroxidation with mutagenic properties. This study investigated whether exposure to 2.45 GHz Wi-Fi radiation, as emitted by a commercial router, could impair sperm quality and cause histopathological damage to rat testes, focusing on duration-dependent effects.

Twenty-four male Sprague-Dawley rats were randomly assigned to four groups (n = 6 per group) and exposed for eight weeks. One group served as the sham-exposed control, while the other three groups were exposed to 2.45-GHz Wi-Fi radiation for 4, 8, or 24 hours daily. The radiation source was a standard commercial Wi-Fi router positioned 20 cm from the cages. It was operated within a shielded chamber to eliminate external electromagnetic interference (EMI). (This setup implicates the investigation of non-thermal Wi-Fi effects, editorial note.) After the exposure period ended, the following assessments were performed: sperm concentration, motility, and viability; serum MDA levels; and histopathological analyses of testicular tissue, including Johnsen’s score, seminiferous tubule diameter, and epithelial height.

In all exposure groups, MDA levels were significantly elevated, indicating increased oxidative stress. This was accompanied by significant deterioration in all sperm quality parameters and significant histopathological alterations. Interestingly, the most severe effects occurred in the group exposed for only 4 hours per day. In contrast, the 8- and 24-hour groups displayed gradual, duration-dependent normalization of the measured parameters over time.

These findings challenge the commonly held assumption that longer exposure durations correlate with greater biological harm. Although the shortest exposure elicited the strongest adverse effects, the authors suggest that compensatory mechanisms may allow for partial regeneration at longer exposure times. However, full recovery was not achieved. The correlation between MDA levels and both sperm quality and histopathology highlights oxidative stress as a potential mechanistic link. The authors call for further research into molecular mechanisms and the impact of combined exposure to different frequencies and environmental stressors.

Editorial note:

This study benefits from a carefully controlled experimental setup that includes shielding, sham-exposed controls, and realistic Wi-Fi parameters. The use of a commercial router enhances the study's relevance, and the focus on non-thermal effects aligns with current exposure guidelines. Graded exposure times enable the dynamic observation of damage and potential adaptation. While 24/7 exposure is less realistic for human comparison, 4- and 8-hour daily exposures are considered representative. Future studies should examine antioxidant signaling cascades and protective enzymes to clarify the underlying mechanisms. The sample size (n = 6) was adequate to detect significance, but increasing the sample size could have provided greater statistical power, especially given the complexity of EMF–tissue interactions. This work offers valuable insights into time-dependent oxidative injury and partial recovery under Wi-Fi exposure. (RH)