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Even though there are contradictory reports regarding the cellular and molecular changes induced by mobile phone emitted radiofrequency radiation (RFR), the possibility of any biological effect cannot be ruled out. In view of a widespread and extensive use of mobile phones, this study evaluates alterations in male germ cell transformation kinetics following RFR exposure and after recovery. Swiss albino mice were exposed to RFR (900 MHz) for 4 h and 8 h duration per day for 35 days. One group of animals was terminated after the exposure period, while others were kept for an additional 35 days post-exposure. RFR exposure caused depolarization of mitochondrial membranes resulting in destabilized cellular redox homeostasis. Statistically significant increases in the damage index in germ cells and sperm head defects were noted in RFR-exposed animals. Flow cytometric estimation of germ cell subtypes in mice testis revealed 2.5-fold increases in spermatogonial populations with significant decreases in spermatids. Almost fourfold reduction in spermatogonia to spermatid turnover (1C:2C) and three times reduction in primary spermatocyte to spermatid turnover (1C:4C) was found indicating arrest in the premeiotic stage of spermatogenesis, which resulted in loss of post-meiotic germ cells apparent from testis histology and low sperm count in RFR-exposed animals. Histological alterations such as sloughing of immature germ cells into the seminiferous tubule lumen, epithelium depletion and maturation arrest were also observed. However, all these changes showed recovery to varied degrees following the post-exposure period indicating that the adverse effects of RFR on mice germ cells are detrimental but reversible. To conclude, RFR exposure-induced oxidative stress causes DNA damage in germ cells, which alters cell cycle progression leading to low sperm count in mice.

BackgroundArsenic, a naturally occurring metalloid is a well-known water contaminant which causes a wide range of serious adverse health effects including cancer upon long-term exposure. Recent studies have shown high arsenic contamination in the ground water of North Eastern states of India including Southern Assam. Smokeless tobacco consumption locally known as “sadagura” is one of the most prevalent life style habit in southern Assam. The present study was undertaken in mice test system in vivo. Mice were exposed to smokeless tobacco (5 mg/kg body weight /day) and sodium arsenite (0.2 mg/kg body weight /day, 2 mg/kg body weight/day) independently and in combination for 90 days.ResultsThe results were compared with groups with only sodium arsenite exposure and groups which were exposed to only smokeless tobacco extract. Genotoxicity was evaluated by studying the incidence of micronucleated polychromatic erythrocytes from bone marrow. Both the tested doses of sodium arsenite induced statistically significant micronucleated polychromatic erythrocytes as compared to control group, however, sodium arsenite and smokeless tobacco extract could not increase the incidence of micronucleated polychromatic erythrocytes as compared to their individual counterparts when treated in combination in mice test system. Germ cell toxicity was evaluated by recording the sperm head abnormalities and total sperm count. Combined treatment of sodium arsenite and smokeless tobacco extract in lower dose induced a significant increase in sperm head abnormality as compared to only sodium arsenite and smokeless tobacco extract. Liver, kidney and intestine tissues were analyzed for various oxidative stress evaluations such as lipid peroxidation (MDA), Glutathione (GSH) and superoxide dismutase (SOD) assay. Sodium arsenite in combination with smokeless tobacco extract show higher genotoxic and germ cell toxic effects as compared to control but not when compared to their individual counterparts.ConclusionImpairment of the sperm head morphology by sodium arsenite and smokeless tobacco extract alone and in combination with lower dose of sodium arsenite could be oxidative stress mediated effects. Besides, combination treatment of both the agents may not produce additive effects related to micronucleated polychromatic erythrocytes induction and decline of total sperm count.

Placental chorioangiomas are benign vascular tumors. Large chorioangiomas cause several obstetric complications, including premature labor, placental abruption, polyhydramnios, fetal hydrops, fetal growth restriction, fetal hepatosplenomegaly, cardiomegaly, congestive heart failure, and fetal death. The neonatal complications are hydrops fetalis, microangiopathic hemolytic anemia, and thrombocytopenia. The cause of perinatal cerebral arterial infarction remains unclear in the majority of cases. Investigators have reported a number of obstetric and neonatal complications in the setting of perinatal stroke, including birth asphyxia, preeclampsia, chorioamnionitis, cardiac anomalies, polycythemia, systemic infection, and genetic thrombophilias. We present a rare case of perinatal cerebral infarction associated with placental chorioangioma.