Department of Biological Science and Technology, Suzhou University of Science and Technology, Suzhou 215009, China.
School of Electronic & Information Engineering, Soochow University, Suzhou 215006, China.
Reprod Toxicol. 2018 Oct;81:229-236. doi: 10.1016/j.reprotox.2018.08.014. Epub 2018 Aug 17.
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/cm 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/RORα. 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/RORα expression induced by RF exposure. Thus, the data provided the evidence that RF-induced inhibition of testosterone synthesis might be mediated through CaMKI/RORα signaling pathway. Capsule: CaMKI/RORα signaling pathway was involved in the inhibition of testosterone synthesis induced by RF exposure.
射频场（RF）暴露据报道会引起睾丸酮产生及其日常节律的不良影响。然而，这种效应背后的机制尚不清楚。在这项研究中，雄性小鼠每天暴露于 1800MHz 射频场（RF，40μW/cm 功率强度和 0.0553W/Kg SAR）2 小时，共 32 天。数据表明，RF 暴露：（i）显著降低睾丸酮水平，（ii）改变睾丸组织中参与其合成的基因的表达（Star、P450scc、P450c17 和 3β-Hsd），（iii）显著降低调节蛋白 CaMKI/RORα。在体外暴露于 RF 的培养原代 Leydig 细胞中也观察到了类似的观察结果。然而，所有这些观察结果都被 CaMK 抑制剂 KN-93 阻断，离子霉素逆转了 RF 暴露引起的细胞内[Ca2+]i 和 CaMKI/RORα表达下调的作用。因此，数据提供了证据表明，RF 诱导的睾丸酮合成抑制可能是通过 CaMKI/RORα信号通路介导的。摘要：CaMKI/RORα 信号通路参与了 RF 暴露诱导的睾丸酮合成抑制。
