1800 MHz radiofrequency fields inhibits testosterone production via CaMKI /RORα pathway.

Highlights • RF exposure reduced testosterone levels and its synthesis genes in mice testis. • RF exposure reduced levels in CamkI/Rorα mRNA/protein expression. • KN-93 blocked the inhibitory effect of RF exposure on testosterone synthesis and regulatory factors of CamkI and Rorα in primary Leydig cells. • Ionomycin reversed the down-regulation effect of RF exposure on intracellular [Ca2+]i and CamkI/Rorα mRNA/protein expression in vitro. Abstract Exposure to radiofrequency fields (RF) has been reported to induce adverse effects on testosterone production and its daily rhythm. However, the mechanisms underneath this effect remain unknown. In this study, male mice were exposed to 1800 MHz radiofrequency fields (RF, 40 μW/cm2 power intensity and 0.0553 W/Kg SAR) 2 h per day for 32 days. The data suggested that RF exposure: (i) significantly reduced testosterone levels, (ii) altered the expression of genes involved in its synthesis (Star, P450scc, P450c17 and 3β-Hsd) in testicular tissue, (iii) significantly reduced regulatory protein CaMKI/ROR α. Similar observations were also made in cultured primary Leydig cells exposed in vitro to RF. However, all of these observations were blocked by CaMK inhibitor, KN-93, and ionomycin reversed the down-regulation effects on intracellular [Ca2+]i and CaMKI/ROR α expression induced by RF exposure. Thus, the data provided the evidence that RF-induced inhibition of testosterone synthesis might be mediated through CaMKI/ROR α signaling pathway. Capsule: CaMKI/RORα signaling pathway was involved in the inhibition of testosterone synthesis induced by RF exposure. [ABSTRACT FROM AUTHOR]