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. 2020 May 26;11:444. doi: 10.3389/fphys.2020.00444

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Copyright © 2020 Ramírez-Barrantes, Carvajal-Zamorano, Rodriguez, Cordova, Lozano, Simon, Díaz, Muñoz, Marchant, Latorre, Castillo and Olivero.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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TRPV1 mediated 17β-estradiol improving of mitochondrial stability during oxidative stress. Time course of H₂O₂-induced cell death (1 mM) following a kinetic model of cell death in HeLa parental (HeLa-P) (A) and st-TRPV1 cells (B) (N = 9). (C,D) Effect of initial pulse of 17β-estradiol on time course of H₂O₂-induced cell death in HeLa Parental (C) and st-TRPV1 (D) cell line (N = 9). (E) Temporal course of ΔΨ in parental and st-TRPV1 cell lines measured by the rationometric probe JC-1. The data shows the first 3 h effect of 1 mM H₂O₂ and 17β-estradiol (N = 9). (F) Activation of caspase 3/7 by H₂O₂ in parental and st-TRPV1 cell lines in presence or absence of 10^–6 M of 17β-estradiol at the first 3 h (N = 6).