Melatonin modulates apoptosis and TRPM2 channels in transfected cells activated by oxidative stress

ÇELİK Ö., NAZIROĞLU M.

PHYSIOLOGY & BEHAVIOR, vol.107, no.3, pp.458-465, 2012 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 107 Issue: 3
  • Publication Date: 2012
  • Doi Number: 10.1016/j.physbeh.2012.09.013
  • Journal Name: PHYSIOLOGY & BEHAVIOR
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Social Sciences Citation Index (SSCI), Scopus
  • Page Numbers: pp.458-465
  • Keywords: Melatonin, Oxidative stress, Ca2+ signaling, TRPM2 channel antagonist, Apoptosis, ADP-RIBOSE, HYDROGEN-PEROXIDE, CALCIUM INFLUX, CA2+ INFLUX, BORATE, POLY(ADP-RIBOSE), MECHANISMS, TOXICITY, LTRPC2
  • Süleyman Demirel University Affiliated: Yes

Abstract

Transient receptor potential melastatin-like 2 (TRPM2) is a non-selective Ca2+ permeable cation channel and is known to be activated by H2O2, one of the most important indicators of intracellular oxidative stress. A neurohormone melatonin may have a modulator role on TRPM2 channels activated by oxidative stress because it is a strong antioxidant. In this study we investigated the effects of melatonin on apoptosis, whole cell currents and Ca2+ influx arising from TRPM2 channels activated by H2O2.