Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence

Chong-Sun Khoi1,2, Jia-Huang Chen1, Tzu-Yu Lin2

  • 1Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 106, Taiwan.

Insights

Ochratoxin A (OTA) causes kidney damage through various molecular pathways. This review details OTA

Area of Science:

  • Toxicology
  • Molecular Biology
  • Nephrology

Background:

  • Ochratoxin A (OTA) is a prevalent mycotoxin in food and feed.
  • OTA exerts multi-organ toxicity, with the kidney as a primary target.
  • Understanding OTA's molecular mechanisms in the kidney is crucial for public health.

Purpose of the Study:

  • To review recent intracellular molecular interactions and signaling pathways in OTA-induced nephrotoxicity.
  • To consolidate knowledge on the molecular mechanisms underlying kidney damage by OTA.
  • To identify potential strategies against OTA toxicity.

Main Methods:

  • Comprehensive literature review of recent studies on OTA nephrotoxicity.
  • Analysis of molecular pathways including pyroptosis, lipotoxicity, and organic anion transport.
  • Examination of cellular processes such as autophagy and the ubiquitin-proteasome system.

Main Results:

  • Key molecular players in OTA nephrotoxicity identified: pyroptosis, lipotoxicity, organic anion transporters, autophagy, ubiquitin-proteasome system, and histone acetyltransferase.
  • Evidence suggests OTA disrupts cellular homeostasis and induces oxidative stress.
  • Various protective strategies reviewed, including ROS reduction, Nrf2 pathway activation, and use of nanoparticles, flavonoids, and metal supplements.

Conclusions:

  • OTA-induced nephrotoxicity involves complex intracellular molecular interactions and signaling pathways.
  • Targeting these pathways offers potential therapeutic strategies against OTA poisoning.
  • Further research into protective agents and mechanisms is warranted.

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