Background: The possible health effects of radio frequency modulated electromagnetic fields (RF-EMF) emitted by mobile phones, cordless phones, base stations and Wi-Fi routers are a growing concern for the public around the world. Aim of the study: to study the possible effects of electromagnetic radiation from mobile phones on oxidant and antioxidant status of testicular tissue and testicular function of male albino rats and its underlying mechanism.Materials and Methods: Twenty male albino rates were divided into two groups: control group A (vehicle driving) and rats were exposed to the phone when the phone was turned off. Exposure to mobile radiation in group B (call mode). Group B was exposed to electromagnetic frequencies for 60 minutes every day for 6 weeks.Results: Mobile radiation exposure in male rats resulted in a significant decrease in serum levels of FSH, LH, testosterone, epididymal sperm count, and sperm motility but weight gain or testicular weight changes were negligible, the testicular Malondialdehyde (MDA) significantly increased when compared with the control group, the testicular antioxidant Superoxide Dismutase (SOD) and Glutathione Peroxidase (GPx) activity showed significant decrease in comparison to control group and there were structural changes in the form of basement membrane rupture, decreased spermatogenic cells, intertubular fibrosis and interstitial cell proliferation.Conclusion: we confirmed the harmful effect of mobile phone radiations on testicular function in male albino rats Key words: Electromagnetic Radiation; testes; rats.

Background: Hyperthyroidism is known to increase the risk of ischemic heart diseases. Octreotide has been reported to attenuate ischemia/reperfusion (I/R) injury. Whether it is useful when ischemic heart disease is accompanied with co-morbidities like hyperthyroidism needs more clarifying. So, this study aimed to explore the effect of octreotide on cardiac I/R injury in hyperthyroid rats and to clarify if Nrf2 activation is involved in this effect. Forty adult female Wistar rats were subdivided into control (euthyroid) (n= 10) and hyperthyroid (n= 30) groups. Rats in hyperthyroid group receivedl-thyroxine (12 mg/L) in drinking water for 35 days, then were randomly divided into three equal subgroups (n= 10): hyperthyroid control positive group, hyperthyroid octreotide treated group, and hyperthyroid octreotide + Nrf2 inhibitor (brusatol) treated group. Isolated hearts were submitted to I/R and evaluated for cardiac hemodynamics and infarct size. Serum T3 and T4, coronary efflux lactate dehydrogenase (LDH) and creatine kinase-myoglobin binding (CK-MB) and cardiac tissue malondialdehyde (MDA) were estimated. Nrf2- regulated gene expressions of HO-1, SOD, GPx, and catalase were assessed.Results: Octreotide administration to hyperthyroid rats improved baseline and post-ischemic recovery of cardiac hemodynamics, decreased the high coronary efflux LDH and CK-MB and tissue MDA, reduced infarction size, and upregulated the decreased antioxidative enzymes HO-1, SOD, GPx, and catalase mRNA expressions in the hyperthyroid I/R rat hearts. The Nrf2 inhibitor brusatol reversed the cardioprotective effect of octreotide in hyperthyroid I/R rat hearts.Conclusion: Octreotide can reduce oxidative stress to effectively alleviate I/R injury in the hyperthyroid rat hearts through upregulation of Nrf2-dependent antioxidative signaling pathways.

Introduction: Cell phones are essential for modern life and their usage becomes prevalent. Worries have increased concerning the harmful effects of their radio-frequency electromagnetic radiation. Liver X receptors (LXRs) are ligand-dependent transcription factors that have important roles in lipid metabolism and inflammation, plus several recently emerging roles. Whether it is useful to overcome the hazardous effects of cell phone radiation needs to be clarified. So, this study aimed to investigate the effect of LXRs activation on testicular changes in rats exposed to electromagnetic radiation. Methods: Thirty adult male Wistar rats were subdivided into control group, experimental group: exposed to cell phone electromagnetic radiation, and treated group: as experimental group and received LXRs agonist T0901317. Serum testosterone (T), Follicle-Stimulating Hormone (FSH), and Luteinizing Hormone (LH), testicular tissue malondialdehyde (MDA) and superoxide dismutase (SOD), and gene expressions of inflammatory and apoptotic markers were assessed. Seminal analysis and testicular histological examination were performed. Results: LXRs activation in rats exposed to cell phone radiation improved the decreased testicular and gonadotrophic hormones, semen quality parameters, tissue SOD, and anti-apoptotic gene expression as well as the elevated tissue MDA, apoptotic and inflammatory gene expressions, and the testicular histological changes induced by exposure to electromagnetic radiation. Conclusion: Exposure to cell phone radiation leads to harmful effects on spermatogenesis and LXRs activation could improve these effects via antioxidant, anti-inflammatory properties in addition to its endocrinal action.