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Induction of HepG2 cell apoptosis by Irgarol 1051 through mitochondrial dysfunction and oxidative stresses

Li Wang1, Bo Liang, Liang Li

  • 1Marine Biology Institute, Shantou University, Shantou, Guangdong 515063, PR China.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|June 1, 2013
PubMed

Insights

Irgarol 1051 exposure damages HepG2 cells, inducing apoptosis via mitochondrial dysfunction and oxidative stress. While low environmental concentrations may be safe for humans, bioaccumulation poses risks to marine predators.

Area of Science:

  • Environmental Toxicology
  • Cell Biology
  • Marine Biology

Background:

  • Irgarol 1051 is a biocide used in antifouling paints.
  • Its environmental impact, particularly on non-target organisms, requires further investigation.

Purpose of the Study:

  • To investigate the toxicological effects of Irgarol 1051 on HepG2 cells.
  • To elucidate the mechanisms of Irgarol 1051-induced cell death.

Main Methods:

  • HepG2 cells were exposed to varying concentrations of Irgarol 1051.
  • Cell viability, morphology, apoptosis markers (Annexin V, caspase activity), mitochondrial membrane potential, cytochrome c release, and reactive oxygen species (ROS) levels were assessed.

Main Results:

  • Irgarol 1051 significantly decreased cell viability and altered cell morphology.
  • Apoptosis was induced via the intrinsic mitochondrial pathway, evidenced by caspase activation, mitochondrial dysfunction, and cytochrome c release.
  • Increased intracellular ROS levels and oxidative stress were observed.

Conclusions:

  • Irgarol 1051 induces apoptosis in HepG2 cells through mitochondrial dysfunction and oxidative stress.
  • While human health risks at environmentally relevant concentrations are uncertain, bioaccumulation may threaten marine ecosystems and top predators.
Keywords:
ApoptosisHepG2 cellIrgarol 1051Mitochondrial membrane potentialReactive oxygen species

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