Selenium Reduces Mobile Phone (900 MHz)-Induced Oxidative Stress, Mitochondrial Function, and Apoptosis in Breast Cancer Cells

Abstract

Exposure to mobile phone-induced electromagnetic radiation (EMR) may affect biological systems by increasing free oxygen radicals, apoptosis, and mitochondrial depolarization levels although selenium may modulate the values in cancer. The present study was designed to investigate the effects of 900 MHz radiation on the antioxidant redox system, apoptosis, and mitochondrial depolarization levels in MDA-MB-231 breast cancer cell line. Cultures of the cancer cells were divided into four main groups as controls, selenium, EMR, and EMR + selenium. In EMR groups, the cells were exposed to 900 MHz EMR for 1 h (SAR value of the EMR was 0.36 ± 0.02 W/kg). In selenium groups, the cells were also incubated with sodium selenite for 1 h before EMR exposure. Then, the following values were analyzed: (a) cell viability, (b) intracellular ROS production, (c) mitochondrial membrane depolarization, (d) cell apoptosis, and (e) caspase-3 and caspase-9 values. Selenium suppressed EMR-induced oxidative cell damage and cell viability (MTT) through a reduction of oxidative stress and restoring mitochondrial membrane potential. Additionally, selenium indicated anti-apoptotic effects, as demonstrated by plate reader analyses of apoptosis levels and caspase-3 and caspase-9 values. In conclusion, 900 MHz EMR appears to induce apoptosis effects through oxidative stress and mitochondrial depolarization although incubation of selenium seems to counteract the effects on apoptosis and oxidative stress.

Effects of Selenium Yeast on Oxidative Stress, Growth Inhibition, and Apoptosis in Human Breast Cancer Cells

“…MSA significantly decreased E2-induced ROS accumulation of T47D breast cancer cells 21 . Selenite also inhibited electromagnetic radiation-induced oxidative stress and reduced the mitochondrial dysfunction in MDA-MB-231 cells 22 . By contrast, some studies showed that selenite exposure induce the apoptosis of cancer cells by producing superoxide radicals 23 , 24 .…”

Protective Role of Selenium Compounds on the Proliferation, Apoptosis, and Angiogenesis of a Canine Breast Cancer Cell Line

“…In addition, oxidative stress-induced apoptosis can be modulated by Ca 2+ release. The apoptosis and oxidative stress levels can be affected by the modulation of Ca 2+ entry through calcium channels, and some channels, such as voltage-gated and transient receptor potential melastatin 2 channels, are activated by oxidative stress, which can be modulated by selenium [8,12]. Selenium has both direct anti-cancer and chemotherapyintensifying effects when combined with conventional chemotherapeutic drugs [27].…”

“…The anti-neoplastic mechanism of selenium compounds is considered to be associated with the prevention of copper-mediated DNA damage, inhibition of oxidation, promotion of cell apoptosis, and immune system regulation. However, the exact mechanisms are still unknown [8][9][10]. Selenium is known to have anti-angiogenic effects, and it can inhibit the growth of malignant cells by exerting cytotoxic activities [11].…”

Alterations in Calcium Signaling Pathways in Breast Cancer

“…The anticancer effects of cisplatin mediated by TRPV1 have to be potentiated by co-application of selenium or alpha-lipoic acid on MCF-7 breast cancer cells [128,129]. Interestingly, selenium was shown to diminish the electromagnetic radiation (900 MHz) effects in MDA-MB-231 breast cancer cell line mediated by TRPV1 activation [130].…”