Cell phones have become an integral part of everyday life. As cell phone usage has become more widespread, concerns have increased regarding the harmful effects of radiofrequency electromagnetic radiation from these devices. The current study was undertaken to investigate the effects of the emitted radiation by cell phones on testicular histomorphometry and biochemical analyses. Adult male Wistar rats weighing 180-200 g were randomly allotted to control, group A (switched off mode exposure), group B (1-hr exposure), group C (2-hr exposure) and group D (3-hr exposure). The animals were exposed to radiofrequency electromagnetic radiation of cell phone for a period of 28 days. Histomorphometry, biochemical and histological investigations were carried out. The histomorphometric parameters showed no significant change (p < .05) in the levels of germinal epithelial diameter in all the experimental groups compared with the control group. There was no significant change (p < .05) in cross-sectional diameter of all the experimental groups compared with the control group. Group D rats showed a significant decrease (p ˂ .05) in lumen diameter compared with group B rats. There was an uneven distribution of germinal epithelial cells in groups B, C and D. However, there was degeneration of the epithelia cells in group D when compared to the control and group B rats. Sera levels of malondialdehyde (MDA) and superoxide dismutase (SOD), which are markers of reactive oxygen species, significantly increased (MDA) and decreased (SOD), respectively, in all the experimental groups compared with the control group. Also sera levels of gonadotropic hormones (FSH, LH and testosterone) significantly decreased (p < .05) in groups C and D compared with the control group. The study demonstrates that chronic exposure to radiofrequency electromagnetic radiation of cell phone leads to defective testicular function that is associated with increased oxidative stress and decreased gonadotropic hormonal profile.

The existence and role of the microbiome in regulating physiological and pathophysiological conditions including metabolism, energy homeostasis, immune tolerance, behavior, obesity, diabetes, and cardiovascular-related diseases is of immense interest. It is now clear that the human placenta is not sterile, but rather colonized with microbes. The placental and vaginal microbiomes are distinct however, the placental microbiome is comparable with the oral microbiome, with a limited variation when compared with the gut microbiome. Pre-eclampsia (PE), a pregnancy-specific hypertensive disorder, remains the leading cause of maternal-fetal morbidity and mortality. This is largely due to the lack of a clear etiology of PE and consequently, diagnostic strategies, and treatment are sub-optimal. The present review focuses on the current understanding of the placental microbiome and its implication in the etiology of PE. It provides a perspective on the alteration of placental microbiome as a possible therapeutic approach in the prevention and management of PE.

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