Autores

Guney M, Ozguner F, Oral B, Karahan N, Mungan T. (2007). 900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat endometrium: protection by vitamins E and C. Toxicol Ind Health 23(7): 411-420.

Background
Studies of the effects of electromagnetic radiation (EMR) on reproductive system in animal experiments and in humans provide controversial results. Some studies indicate that oxidative stress, which promotes production of reactive oxygen species (ROS), may play a role in the biological effects of this radiation.

Objective
The aim of the study was to examine 1) if oxidative stress plays a role in possible 900 MHz mobile phone-induced damage to endometrium, the key tissue of reproductive system, and 2) whether or not co-administration of vitamins E and C, which have antioxidant properties, decreases or inhibits endometrial damage potentially resulted from 900 MHz EMR.

Methods

Thirty-two sexually mature female Wistar-albino rats (16 weeks old, 170-200 g) were randomly grouped as follows:

  1. Control group (without stress and EMR; Group I).
  2. Sham-operated animals injected with isotonic saline solution and placed in the tube with the same environmental room conditions as the exposure groups, but without exposure to EMR (exposure device off; Group II).
  3. Rats exposed to 900 MHz EMR (EMR group; Group III).
  4. 900 MHz EMR exposed + vitamins E and C treated group (EMR+ Vit group; Group IV).

EMR exposure was conducted for 30 minutes a day for 30 days at specific absorption rate (SAR) between 0.016 and 4 W/kg. Vitamin E and C were injected at doses of 50 mg/kg and 20 mg/kg body weight respectively. Biochemical analyses were conducted to determine endometrial tissue levels of nitric oxide (NO, an oxidant product) and malondialdehyde (MDA, an index of lipid peroxidation), as well as activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). Histopathological examinations of the uterus were conducted by two independent experts who were unaware of the treatment group of the experimental animals. Experts examined the differences between the groups.

Results

Endometrial tissue levels of MDA and NO in the EMR exposed group were higher than those in the sham operated and control groups (P<0.01). Vitamins C and E administration (EMR + Vit group) significantly reduced MDA and NO levels compared with the EMR group. In the EMR exposed group, a significant decrease in activities of antioxidant enzymes (SOD, GSH-Px and CAT) in endometrial tissue was observed compared to the sham-exposed and control groups (P<0.01). Activities of antioxidant enzymes in the vitamins E and C administered animals (EMR + Vit group) were significantly higher than those in the EMR group (P<0.01). Histopathological changes occurred in the EMR group. Significantly lower level of apoptosis and inflammatory cell infiltration was observed in the EMR + Vit group.

Interpretation

The observed changes in the MDA and NO levels and in the activities of antioxidant enzymes in the endometrium of the EMR exposed animals may be regarded as an indicator of the EMR-induced oxidative stress, which plays a role in the pathogenesis of endometrial damage. It has been shown in other studies that long-term exposure to EMR may cause histopathological changes in brain, skin and testis. The authors note, however, that biological effects of mobile phone exposure may be variable depending on exposure periods, conditions, species and tissues. Also, it is difficult to extrapolate effects from rodents to humans because the entire body of a rat is exposed whereas for a person using a mobile telephone, only the skin near the region of the uterus that is close to the telephone would be exposed.
Though some information exists on inhibition of biological effects of EMR exposure by vitamin E administration, little data are available on antioxidant features of the combination of vitamins E and C in the endometrial tissue. The present study demonstrates that vitamins E and C inhibit the EMR-induced endometrial damage and supports the hypothesis that superoxide radicals are involved in its pathogenesis.

Conclusion

The results of this study demonstrate that there is an oxidative stress-induced impairment in endometrial tissue after mobile phone exposure. The modulation of oxidative stress with a combination of vitamins E and C reduces the 900 MHz mobile phone induced endometrial damage in rats both at the biochemical and the histological levels. Further studies with different frequencies and exposure periods are needed in order to prove the protective effect of vitamins E and C on oxidative stress and histopathologic damage in the endometrium due to EMR.



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