Bisphenol A-Induced Cell Proliferation and Mitochondrial Oxidative Stress Are Diminished via Modulation of TRPV1 Channel
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Bisphenol A-Induced Cell Proliferation and Mitochondrial Oxidative Stress Are Diminished via Modulation of TRPV1 Channel in Estrogen Positive Breast Cancer Cell by Selenium Treatment Kadriye Görkem Ulu Güzel 1 & Mustafa Nazıroğlu 2,3
&
Derya Ceyhan 4
Received: 3 January 2020 / Accepted: 27 January 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Cancer cell proliferation and apoptosis are induced by overload Ca2+ entry. Transient receptor potential vanilloid 1 (TRPV1) as a Ca2+ permeable cation channel is activated by capsaicin and reactive oxygen species (ROS), although it is blocked by capsazepine and sodium selenite (Na-Se). Bisphenol A (BPA) induces estrogenic action and further stimulates the proliferation of estrogen receptor positive MCF-7 cell through excessive production ROS and Ca2+ influx. However, whether or not Na-Se can influence BPA-induced oxidative stress and apoptosis through modulation of TRPV1 in breast cancer cells has not drawn much attention. The MCF-7 and MDA-MB-231 breast cancer cells were divided into four treatment groups as control, Na-Se (1 μM for 2 h), and BPA (0.1 mM for 24 h) and BPA + Na-Se. The Na-Se reduced BPA-induced increase of cell number, mitochondria oxidative stress, and TRPV1 channel activity modulation of MCF-7 cells, which was proved by the suppression of cell viability, excessive ROS production, mitochondrial membrane depolarization, lipid peroxidation, early apoptosis (Annexin-V), late apoptosis (propidium iodide) and upregulation of reduced glutathione, glutathione peroxidase, and cell death (propidium iodide/ Hoechst rate). The similar effects of Na-Se were observed in the MCF-7 cells by capsazepine treatment. However, the effects of BPA were not observed in the MDA-MB-231 breast cancer cells. In conclusion, cell proliferative and oxidant effects of BPA were increased by activation of TRPV1, but its action on the values was decreased by the Na-Se treatment. The results may be a good set of preliminary data for designing animal studies on estrogenic effect of bisphenol A and antiestrogenic of selenium. Keywords Apoptosis . Bisphenol A . Breast cancer cells . Oxidative stress . Selenium . TRPV1 channel
Introduction Bisphenol A (BPA) as a synthetic compound contains two hydroxyphenyl groups. BPA used several live materials such as baby feeding bottles, food packaging, and medical facilities. Hence, BPA is one of popular environmental toxicant [1,
* Mustafa Nazıroğlu [email protected] 1
Department of Pedodontics, Faculty of Dentistry, Adnan Menderes University, Aydın, Turkey
2
Neuroscience Research Center, Suleyman Demirel University, 32260 Isparta, Turkey
3
Drug Discovery and Development Research Group, BSN Health, Analysis and Innovation Ltd. Inc. Teknokent, Goller Bolgesi Teknokenti, Isparta, Turkey
4
Department of Pedodontics, Faculty of Dentistry, Suleyman Demirel University, Isparta, Turkey
2]. Thus, its continuous exposure in the environment has raised major public health concerns in cancer development [3].
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