The effect of 20-week continuous 60 Hz magnetic field exposure on testicular function in sprague-dawley rats.

Accumulating evidence does not yet confirm the effect of power line frequency magnetic field (MF) on human health and fertility. We recently reported that, at continuous 60 Hz MF exposure in mice, the dose given as magnetic flux density (tesla; T) and duration of exposure was related to induce testicular germ cell apoptosis. We aimed to characterize the effect of a 20-week continuous exposure to 60 Hz MF on the motility, morphology, and number of sperm as well as the apoptosis of testicular germ cell in rats. Sprague-Dawley rats were exposed for 20 weeks to 60 Hz MF of 2, 20, or 200 µT for 24 h/day with rats exposed to sham conditions, serving as the control. The exposure to 60 Hz MF of 2 and 20 µT had no effects on testicular in this study. The exposure to 60 Hz MF of 200 µT for 20 weeks induced increases of the apoptotic cells (P < 0.001) in germ cells and decreases of sperm numbers (P < 0.05). However, the MF did not significantly affect the body or testis mass, seminiferous tubule diameter, or the motility or morphology of sperm. This study concluded that exposure to 60 Hz MF of 200 µT can increase testicular germ cell apoptosis, especially spermatogonia, and reduce sperm count. Also compared to previous mice studies, rats are less sensitive than mice to exposure to 60 Hz MF. Bioelectromagnetics. 39:539-546, 2018. © 2018 Wiley Periodicals, Inc.

Tyr42 phosphorylation of RhoA GTPase promotes tumorigenesis through nuclear factor (NF)-κB.

Dysregulation of reactive oxygen species (ROS) levels is implicated in the pathogenesis of several diseases, including cancer. However, the molecular mechanisms for ROS in tumorigenesis have not been well established. In this study, hydrogen peroxide activated nuclear factor-κB (NF-κB) and RhoA GTPase. In particular, we found that hydrogen peroxide lead to phosphorylation of RhoA at Tyr42 via tyrosine kinase Src. Phospho-Tyr42 (p-Tyr42) residue of RhoA is a binding site for Vav2, a guanine nucleotide exchange factor (GEF), which then activates p-Tyr42 form of RhoA. P-Tyr42 RhoA then binds to IκB kinase γ (IKKγ), leading to IKKß activation. Furthermore, RhoA WT and phospho-mimic RhoA, RhoA Y42E, both promoted tumorigenesis, whereas the dephospho-mimic RhoA, RhoA Y42F suppressed it. In addition, hydrogen peroxide induced NF-κB activation and cell proliferation, along with expression of c-Myc and cyclin D1 in the presence of RhoA WT and RhoA Y42E, but not RhoA Y42F. Indeed, levels of p-Tyr42 Rho, p-Src, and p-65 are significantly increased in human breast cancer tissues and show correlations between each of the two components. Conclusively, the posttranslational modification of as RhoA p-Tyr42 may be essential for promoting tumorigenesis in response to generation of ROS.

Familial Creutzfeldt-Jakob disease with a mutation at codon 180 presenting with an atypical phenotype.

The clinical features of familial Creutzfeldt-Jakob disease (fCJD) with a mutation at codon 180 (V180I) are less typical than those of patients with sporadic CJD. We describe a patient with pathologically confirmed CJD carrying the V180I mutation who had atypical cerebrospinal fluid and electroencephalography findings. Similar to other prion protein mutations, this report suggests that the V180I mutation is not the exclusive determinant of the phenotype.