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Hexavalent Chromium Causes Apoptosis and Autophagy by Inducing Mitochondrial Dysfunction and Oxidative Stress in

Hao Li1, Jingjing Shi1, Haihang Gao1

  • 1College of Veterinary Medicine, Veterinary clincal medicine laboratory, Huazhong Agricultural University, 1 Shizishan Street, Wuhan, CA, 430070, People's Republic of China.

Biological Trace Element Research
|August 14, 2021
PubMed

Insights

Hexavalent chromium (Cr(VI)) exposure induces heart cell death (apoptosis) and self-eating processes (autophagy) in broilers. This occurs by damaging mitochondria and increasing oxidative stress, highlighting Cr(VI) cardiac toxicity.

Area of Science:

  • Environmental Toxicology
  • Cardiovascular Science
  • Cell Biology

Background:

  • Hexavalent chromium (Cr(VI)) is a prevalent environmental toxicant with known adverse effects.
  • Cardiac toxicity of Cr(VI) in poultry, specifically broilers, is not well understood.
  • Mitochondrial dysfunction is a key factor in heart disease development, particularly following toxicant exposure.

Purpose of the Study:

  • To investigate the role of mitochondrial dysfunction in Cr(VI)-induced apoptosis and autophagy in broiler cardiomyocytes.
  • To elucidate the molecular mechanisms underlying Cr(VI) cardiac toxicity in broilers.

Main Methods:

  • Broiler cardiomyocytes were exposed to varying concentrations of potassium dichromate (Cr(VI)).
  • Assessed levels of reactive oxygen species (ROS), apoptosis rates, and expression of apoptosis-related genes (Bax, p53, Bcl-2).
  • Analyzed autophagy markers (LC3-I, LC3-II, Beclin1, mTOR, p62/SQSTM1) and mitochondrial function (membrane potential, dynamics genes: SIRT1, SIRT3, Mfn2).

Main Results:

  • Cr(VI) exposure dose-dependently increased ROS production and apoptosis rates.
  • Apoptosis gene expression shifted towards pro-apoptotic (Bax, p53) and away from anti-apoptotic (Bcl-2).
  • Autophagy markers (LC3-II/LC3-I ratio, Beclin1) increased, while mTOR and p62/SQSTM1 decreased, indicating active autophagy.
  • Mitochondrial membrane potential decreased, and expression of mitochondrial dynamics genes (SIRT1, SIRT3, Mfn2) was significantly reduced.

Conclusions:

  • Cr(VI) induces myocardial apoptosis and autophagy in broilers.
  • Mitochondrial dysfunction and oxidative stress are key mechanisms mediating Cr(VI) cardiac toxicity.
  • Findings reveal Cr(VI) as a significant threat to broiler cardiac health.

Keywords:
ApoptosisAutophagyBroiler cardiomyocytesHexavalent chromiumMitochondrial dysfunctionOxidative stress

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