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Ochratoxin A-induced cytotoxicity, genotoxicity and reactive oxygen species in kidney cells: An integrative approach

João G Costa1, Nuno Saraiva2, Patrícia S Guerreiro3

  • 1CBIOS, Universidade Lusófona Research Center for Biosciences & Health Technologies, Campo Grande 376, 1749-024 Lisboa, Portugal; Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Professor Gama Pinto, 1649-003 Lisboa, Portugal; Department of Biomedical Sciences, University of Alcalá, Ctra. Madrid-Barcelona Km. 33.600, 28871 Alcalá de Henares, Madrid, Spain.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|December 3, 2015
PubMed

Insights

Ochratoxin A (OTA) causes kidney cell damage and DNA lesions, partly due to reactive oxygen species (ROS). A superoxide dismutase mimic (SODm) reduced these OTA-induced effects, suggesting oxidative stress involvement.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Cell Biology

Background:

  • Ochratoxin A (OTA) is a nephrotoxic and potentially carcinogenic mycotoxin.
  • The precise molecular mechanisms behind OTA's toxicity remain unclear.
  • Investigating the role of reactive oxygen species (ROS) is crucial for understanding OTA's effects.

Purpose of the Study:

  • To investigate the toxicological effects of Ochratoxin A (OTA) in Vero kidney cells.
  • To elucidate the contribution of reactive oxygen species (ROS) to OTA-induced toxicity.
  • To utilize a superoxide dismutase mimic (SODm) as a tool to assess oxidative stress involvement.

Main Methods:

  • Cytotoxicity assays (crystal violet, neutral red, LDH leakage).
  • Genotoxicity assessment (micronuclei formation, comet assay).
  • Apoptosis evaluation and ROS detection (DHE assay) with and without SODm.

Main Results:

  • OTA exhibited concentration- and time-dependent cytotoxicity and genotoxicity.
  • OTA induced DNA lesions and apoptosis, which were partially attenuated by SODm.
  • SODm reduced ROS accumulation, indicating partial involvement of oxidative stress.

Conclusions:

  • Reactive oxygen species (ROS) partially mediate Ochratoxin A's cytotoxicity and genotoxicity.
  • Other mechanisms likely contribute to OTA's overall deleterious effects.
  • Superoxide dismutase mimics show potential in mitigating OTA-induced oxidative stress.
Keywords:
AntioxidantsCytotoxicityGenotoxicityMnTnHex-2-PyPOchratoxin AReactive oxygen species

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