OBJECTIVES: To determine the effects of Egb761 on testicular tissues and semen parameters in rats exposed to cellphone waves. BACKGROUND: EGb761 has antioxidant properties as a free-radical scavenger. Cellphone electromagnetic radiation (EMR) induces oxidative stress in cells. METHODS: Twenty-one Wistar albino male adult rats were divided into three groups (control, experimental, treatment), including seven rats in each. The experimental and treatment groups were exposed to cellphone EMR (0.96 W/kg) for six weeks (4 hrs/day). Egb761 (100 mg/kg/day) was also added to the treatment. Testes, epididymal semen and blood plasma were used for analysis. RESULTS: Exposure to cellular phone radiation resulted in a signifi cant impairment in testicular morphometry and histological structure, reduction of total and motile sperm numbers and plasma testosterone level. Egb761 administration improved testicular damage and led to a marked increase in plasma testosterone levels and total and motile sperm numbers. CONCLUSION: Male reproductive system is susceptible to cellphone radiation. Cellphone waves induce toxic effects in testicular tissues, impair spermatogenesis and cause an imbalance in testosterone hormone levels. Egb761 ameliorated these toxic effects by reversing testicular tissue damage, restoring normal spermatogenesis and hormone levels. This suggests that Egb761 is a potential therapeutic agent against EMR-induced male reproductive toxicity (Tab. 3, Fig. 6, Ref. 45). Text in PDF www.elis.sk.

Modafi nil, is a wake-promoting drug approved by Food and Drugs Administration (FDA) for narcolepsy and sleep-apnoe syndrome. Although the mechanism underlying its arousal action remains elusive, it is known to increase glutamatergic, histaminergic, noradrenergic and dopaminergic transmission and decrease GABA release in different regions of the brain, which are all known to be involved in pathophysiology of epilepsy. In the present study, the effects of modafi nil on pentylenetetrazol (PTZ) induced convulsive epilepsy were investigated in rats. Five experimental groups were formed for this purpose and each group was administered fi ve different doses of modafi nil (1, 2, 4, 45, 180 mg/kg, i.p) for seven days. All groups were administered PTZ (80 mg/kg, i.p) 2 hours after the fi nal dose and the epileptic seizure activity was evaluated. According to the results; we detected that modafi nil delayed the onset of the fi rst myoclonic jerk and decreased the total major seizure period between 2-180 mg/kg doses and did not affect the major seizure onset period at any of the doses administrated. These results imply that modafi nil exerts a dose dependent antiepileptic effect on PTZ induced convulsive epilepsy in rats (Tab.