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Cytotoxicity of T-2 toxin and its metabolites determined with the neutral red cell viability assay

H Babich1, E Borenfreund

  • 1Laboratory Animal Research Center, Rockefeller University, New York, New York 10021.

Insights

The neutral red assay quantified T-2 mycotoxin potency in human cells. Human melanoma cells were most sensitive, showing T-2 mycotoxin is more potent than its metabolites.

Area of Science:

  • Toxicology
  • Cell Biology
  • Mycotoxin Research

Background:

  • T-2 mycotoxin is a potent trichothecene mycotoxin produced by Fusarium species.
  • Mycotoxins pose significant risks to human and animal health through contaminated food and feed.
  • Understanding the cytotoxic effects of T-2 mycotoxin and its metabolites is crucial for risk assessment.

Purpose of the Study:

  • To quantitate the cytotoxic potency of T-2 mycotoxin and its metabolites using the neutral red assay.
  • To identify human cell lines with varying sensitivity to T-2 mycotoxin.
  • To establish the relative potency of T-2 mycotoxin compared to its metabolites HT-2, T-2 triol, and T-2 tetraol.

Main Methods:

  • Utilized the neutral red (NR) cell viability assay.
  • Tested various human cell types, including the SK-Mel/27 melanoma cell line and the HepG2 hepatoma cell line.
  • Determined midpoint cytotoxicity values (EC50) for T-2 mycotoxin.

Main Results:

  • The human melanoma SK-Mel/27 cell line exhibited the highest sensitivity to T-2 mycotoxin, with a midpoint cytotoxicity value of 2.8 ng/ml.
  • In the human hepatoma HepG2 cell line, the potency sequence was determined as T-2 > HT-2 > T-2 triol > T-2 tetraol.
  • This indicates T-2 mycotoxin is significantly more potent than its primary metabolites.

Conclusions:

  • The neutral red assay is effective for assessing T-2 mycotoxin cytotoxicity across different human cell lines.
  • Human melanoma cells (SK-Mel/27) are particularly sensitive to T-2 mycotoxin.
  • T-2 mycotoxin demonstrates greater cytotoxicity than its metabolites HT-2, T-2 triol, and T-2 tetraol, highlighting its primary toxicological significance.

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