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Multiple pathways are involved in palmitic acid-induced toxicity.

Eun-Jung Park1, Ah Young Lee2, Sungjin Park2

  • 1Department of Molecular Science and Technology, Ajou University, Suwon 443-749, Republic of Korea.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|February 4, 2014
PubMed
Summary

Palmitic acid (PA) accumulation in liver cells triggers cell death via oxidative stress, mitochondrial dysfunction, and ER stress, activating apoptosis and autophagy. Blocking autophagy accelerates PA-induced liver cell damage.

Keywords:
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Area of Science:

  • Hepatology
  • Cell Biology
  • Toxicology

Background:

  • Palmitic acid (PA), a common saturated fatty acid, can accumulate in cells.
  • Cellular accumulation of PA is linked to various toxic effects.
  • Understanding the precise toxic mechanisms of PA is crucial for liver health.

Purpose of the Study:

  • To elucidate the toxic mechanism of palmitic acid (PA) accumulation in human Chang liver cells.
  • To investigate the roles of apoptosis, necroptosis, autophagy, and ER stress in PA-induced liver cell injury.
  • To determine the impact of oxidative stress on PA toxicity.

Main Methods:

  • Exposure of human Chang liver cells to palmitic acid (PA).
  • Assessment of cellular viability, ATP levels, and cell cycle progression.
  • Measurement of reactive oxygen species (ROS) generation and SOD-2 expression.
  • Analysis of protein levels associated with apoptosis, necroptosis, autophagy, and ER stress.
  • Pharmacological inhibition of caspases, p53, necroptosis, ER stress, and autophagy.

Main Results:

  • PA exposure led to mitochondrial and ER dilation, increased ROS production, and elevated SOD-2 expression.
  • Cell viability decreased, accompanied by ATP reduction and G2/M phase arrest.
  • PA enhanced proteins involved in apoptosis, necroptosis, autophagy, and ER stress.
  • Inhibition of caspases, p53, necroptosis, or ER stress partially rescued PA-induced cytotoxicity and cell cycle changes.
  • Blocking autophagy exacerbated PA-induced cytotoxicity and cell cycle alterations.

Conclusions:

  • Palmitic acid induces liver cell apoptosis and autophagy via oxidative stress, mitochondrial dysfunction, and ER stress.
  • Inhibition of apoptosis, necroptosis, p53, or ER stress can mitigate PA-induced liver cell damage.
  • Autophagy inhibition accelerates PA-induced cytotoxicity and cell cycle dysregulation, highlighting its protective role in this context.