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Resveratrol-induced mitochondrial dysfunction and apoptosis are associated with Ca2+ and mCICR-mediated MPT

Xiaodong Ma1, Xuemei Tian, Xingxu Huang

  • 1Instrumental Analysis & Research Center, Southern Medical University, Guangzhou 510515, China.

Molecular and Cellular Biochemistry
|March 31, 2007
PubMed

Insights

Resveratrol triggers cancer cell death by opening mitochondrial pores, a process dependent on calcium signaling. Targeting calcium release from mitochondria may offer new cancer prevention strategies.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Resveratrol, a natural antioxidant, exhibits cancer chemopreventive properties by inducing apoptosis.
  • Apoptosis can be triggered through various pathways, including the mitochondrial pathway.

Purpose of the Study:

  • To investigate the role of mitochondrial permeability transition (MPT) and intracellular calcium (Ca2+) in resveratrol-induced apoptosis of HepG2 cells.
  • To elucidate the mechanism by which resveratrol affects mitochondrial function and cell death.

Main Methods:

  • Assessing mitochondrial membrane potential (DeltaPsi(m)) collapse and cytochrome c (Cyt.c) release in HepG2 cells treated with resveratrol.
  • Measuring intracellular Ca2+ levels and evaluating the synergistic effect of resveratrol and Ca2+ on MPT induction.
  • Utilizing ruthenium red (RR), an mCICR inhibitor, to determine its impact on resveratrol-induced MPT and apoptosis.

Main Results:

  • Resveratrol induced HepG2 cell apoptosis and mitochondrial dysfunction, characterized by MPT induction, DeltaPsi(m) collapse, and Cyt.c release.
  • Resveratrol caused a rapid and sustained increase in intracellular Ca2+, which was crucial for compromising mitochondrial function and initiating apoptosis.
  • Ca2+ is necessary for resveratrol-induced MPT opening, and mCICR plays a key role, as evidenced by RR's ability to prevent MPT and apoptosis.

Conclusions:

  • Resveratrol-induced HepG2 cell apoptosis is dependent on MPT induction, which is modulated by intracellular Ca2+ levels.
  • Calcium-induced calcium release from mitochondria (mCICR) is a critical mediator of resveratrol's apoptotic effects.
  • Modulating mCICR and the Ca2+ threshold for MPT opening presents a potential therapeutic target for controlling resveratrol-induced apoptosis in cancer therapy.

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