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Deoxynivalenol induced oxidative stress and genotoxicity in human peripheral blood lymphocytes

Wei Yang1, Miao Yu1, Juan Fu1

  • 1Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China; Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China.

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|December 21, 2013
PubMed

Insights

Deoxynivalenol (DON) causes cytotoxicity and genotoxicity in human lymphocytes by inducing oxidative damage. This mycotoxin impairs DNA repair mechanisms, highlighting potential health risks from DON exposure.

Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Deoxynivalenol (DON) is a prevalent mycotoxin found in food and feed.
  • Mycotoxins pose significant risks to human and animal health.
  • Understanding DON's cellular and molecular effects is crucial for risk assessment.

Purpose of the Study:

  • To evaluate the cytotoxicity, genotoxicity, and oxidative damage induced by DON in human peripheral blood lymphocytes.
  • To investigate the underlying mechanisms of DON-induced cellular damage.
  • To assess the impact of DON on DNA repair pathways.

Main Methods:

  • Human lymphocytes were exposed to varying concentrations of DON (0-500 ng/mL) for 6, 12, and 24 hours.
  • Cell viability, membrane integrity, and DNA damage were assessed using cellular assays.
  • Oxidative stress markers (lipid peroxidation, 8-OHdG, ROS) were measured.
  • Gene and protein expression of DNA repair enzymes and HO-1 were analyzed via RT-PCR and Western Blot.

Main Results:

  • DON significantly decreased cell viability and caused damage to cell membranes, chromosomes, and DNA.
  • Exposure to DON induced lipid peroxidation and elevated levels of 8-OHdG and reactive oxygen species (ROS).
  • DON enhanced mRNA/protein expression of DNA repair genes and HO-1 at 6 hours but inhibited them at 24 hours.

Conclusions:

  • DON exhibits significant cytotoxicity and genotoxicity in human lymphocytes.
  • The mechanism involves oxidative DNA damage and impaired antioxidase activity.
  • DON interferes with DNA repair pathways, potentially leading to long-term genetic instability.
Keywords:
2′, 7′-dichlorofluorescein5-methylcytosine8-OHdG8-hydroxydeoxyguanosineBERCyt BDCFH-DADNA repairDONDeoxynivalenolGSHGSSGGenotoxicityHO-1HPLCHbHuman lymphocytesL-glutathione oxidizeL-glutathione reducedLC/MSMDA, Lipid peroxidationMMCMNMalonaldehydeOECDOrganization for Economic Cooperation and DevelopmentOxidative damagePHAROSRT-PCRSCEX-ray repair cross-complementing protein-1XRCC-1base excision repaircytochalasin BdeoxynivalenolhOGG-1heme oxygenase-1hemoglobinhigh-performance liquid chromatographyhuman oxoguanine glycosylase-1liquid chromatography/mass spectrometrym5dCmicronucleus cellmitomycin Cphytohemagglutininreactive oxygen speciesreverse transcription-polymerase chain reactionsister chromatid exchange

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