There is a growing public concern about the potential human health hazard caused by exposure to electromagnetic radiation (EMR). The objective of this study is to investigate the effects of 2450 mhz electromagnetic field on apoptosis and histopathological changes on rat testis tissue. Twelve-week-old male Wistar Albino rats were used in this study. Eighteen rats equally divided into three different groups which were named group I, II and III. Cage control (group I), sham control (group II) and 2.45 GHz EMR (group III) groups were formed. Group III were exposed to 2.45 GHz EMR, at 3.21 W/kg specific absorption rate for 60 minutes/ day for 28 days. There was no difference among the groups for the diameter of the seminiferous tubules, pyknotic, karyolectic and karyotic cells. However, the number of Leydig cells of testis tissue of the rats in group III was significantly reduced comparing with the group I (p < 0.05). Estimation of spermatogenesis using the Johnsen testicular biopsy score revealed that the difference between groups is statistically significant. The level of TNF-α, Caspase-3 and Bcl-2 were compared, and no significant difference was found between the groups. When Bax apoptosis genes and Caspase-8 apoptosis enzyme were compared, there were significant differences between the groups (p < 0.05). Electromagnetic field affects spermatogenesis and causes to apoptosis due to the heat and other stress-related events in testis tissue.

Wireless devices have become part of everyday life and mostly located near reproductive organs while they are in use. The present study was designed to determine the possible protective effects of melatonin on oxidative stress-dependent testis injury induced by 2.45-GHz electromagnetic radiation (EMR). Thirty-two rats were equally divided into four different groups, namely cage control (A1), sham control (A2), 2.45-GHz EMR (B) and 2.45-GHz EMR+melatonin (C). Group B and C were exposed to 2.45-GHz EMR during 60 min day(-1) for 30 days. Lipid peroxidation levels were higher in Group B than in Group A1 and A2. Melatonin treatment prevented the increase in the lipid peroxidation induced by EMR. Also reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) levels in Group D were higher than that of exposure group. Vitamin A and E concentrations decreased in exposure group, and melatonin prevented the decrease in vitamin E levels. In conclusion, wireless (2.45 GHz) EMR caused oxidative damage in testis by increasing the levels of lipid peroxidation and decreasing in vitamin A and E levels. Melatonin supplementation prevented oxidative damage induced by EMR and also supported the antioxidant redox system in the testis.

An imbalance between oxidative stress and antioxidative capacity may play an important role in the development and progression of bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD). We carried out a study to assess the systemic oxidant-antioxidant status during the exacerbation and the stable period in patients with BA and COPD. A total of 33 patients, 16 with BA and 17 with COPD were included in the study. During the exacerbation and the stable periods, levels of malondialdehyde (MDA), activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GRd), and catalase (CAT) in erythrocytes and serum melatonin concentrations were investigated. Blood counts, respiratory functions, and blood gases of the patients were also performed. During an exacerbation period of BA, despite the decreases in GSH-Px, GRd and melatonin levels, MDA and CAT levels, and the white blood cell count, the percentage of eosinophils were significantly higher than in the stable period. Also, it was found that FEV(1)/L (where FEV(1) is the forced expiratory volume in 1 s), FVC/L (where FVC is forced vital capacity), PEF/L/s (where PEF is peak expiratory flow), pO(2) (where pO(2) is oxygen pressure) levels increased during the stable period in patients with BA. MDA and SOD values were higher in the exacerbation period than in the stable period although GSH-Px, GRd, melatonin, pH, and pO(2) values were lower in the exacerbation period than in the stable period. The blood counts and the respiratory function tests did not change between the exacerbation and the stable period of patients with COPD significantly. In conclusion, we observed that oxidative stress in the exacerbation period of patients with BA and COPD increased whereas the antioxidant enzymes and melatonin values reduced. The episodes of BA or COPD might be associated with elevated levels of oxidative stress.

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L-carnitine and selenium seem to have protective effects on the 2.45 GHz-induced decrease of the vitamins by supporting antioxidant redox system. L-carnitine on the vitamin concentrations seems to more protective affect than in selenium.