Resveratrol diminishes bisphenol A-induced oxidative stress through TRPM2 channel in the mouse kidney cortical collecting duct cells.


Çiğ B., Yildizhan K.

Journal of receptor and signal transduction research, ss.1-14, 2020 (SCI Expanded İndekslerine Giren Dergi) identifier

  • Cilt numarası:
  • Basım Tarihi: 2020
  • Doi Numarası: 10.1080/10799893.2020.1769657
  • Dergi Adı: Journal of receptor and signal transduction research
  • Sayfa Sayıları: ss.1-14

Özet

Bisphenol A (BisPH-A) is a latent danger that threatens our health, which we frequently exposure in

our modern life (e.g. the widespread use of drinking water in plastic pet bottles). But the BisPH-A

induced transient receptor potential melastatin 2 (TRPM2)-mediated oxidative stress and apoptosis in

these cells has not been studied yet. Calcium (Ca2þ) plays an important role in a versatile intracellular

signal transduction that works over a wide range to regulate oxidative stress processes. TRPM2 is activated

by oxidative stress and it has emerged as an important Ca2þ signaling mechanism in a variety

of cells, contributing many cellular functions including cell death. Resveratrol (RESV), which belongs to

the polyphenol group, acts as an antioxidant, eliminating cellular oxidative stress and increasing the

body’s resistance to diseases. The current study aimed to elucidate the effect of antioxidant resveratrol

on TRPM2-mediated oxidative stress induced by BisPH-A exposure in the mouse kidney cortical collecting

duct cells (mpkCCDcl4). The cells were divided into four groups as control, resveratrol (50 mM for

24 h), BisPH-A (100 mM for 24 h) and BisPH-AþRESV. Intracellular free Ca2þ concentrations and TRPM2

channel currents were high in BisPH-A treated cells, but decreased with resveratrol treatment. In addition,

BisPH-A induced mitochondrial membrane depolarization, reactive oxygen species (ROS), caspase

3, caspase 9 and apoptosis values were decreased by the resveratrol treatment. In conclusion, resveratrol

protected cells from BisPH-A induced oxidative damage. In this study, we showed that TRPM2

channel mediates this protective effect of resveratrol.