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Apoptotic cellular damage in mice after T-2 toxin-induced acute toxicosis

T Ihara1, M Sugamata, M Sekijima

  • 1Department of Pathology, Institute of Tochigi Clinical Pathology, Tochigi, Japan.

Natural Toxins
|January 1, 1997
PubMed

Insights

T-2 toxin, a mycotoxin, induces programmed cell death (apoptosis) in mouse thymus, spleen, and liver. This cellular destruction, marked by DNA fragmentation, highlights T-2 toxin

Area of Science:

  • Toxicology
  • Cell Biology
  • Immunology

Background:

  • T-2 toxin is a trichothecene mycotoxin known to cause cellular damage.
  • Understanding the precise mechanisms of T-2 toxin-induced cell death is crucial for risk assessment.
  • Previous in vitro studies suggested T-2 toxin induces apoptosis.

Purpose of the Study:

  • To investigate the in vivo mechanism of T-2 toxin-induced cellular death.
  • To examine the effects of T-2 toxin on thymus, spleen, and liver tissues.
  • To determine the role of Kupffer cells in the clearance of apoptotic cells.

Main Methods:

  • Histopathological examination of thymus, spleen, and liver tissues.
  • Electron microscopy to identify cellular ultrastructure and apoptotic bodies.
  • In situ nick translation (Tunel method) to detect DNA fragmentation.

Main Results:

  • Massive cellular destruction with chromatin condensation and apoptotic bodies observed in thymus and spleen 12 hours post-T-2 toxin administration.
  • Apoptotic cellular lesions induced in the liver within 2 hours, with Kupffer cells phagocytosing apoptotic bodies.
  • DNA fragmentation detected in thymus, spleen, and liver shortly after T-2 toxin exposure.

Conclusions:

  • T-2 toxin is a potent inducer of apoptotic cell death in vivo across thymus, spleen, and liver.
  • Apoptosis induction in the liver is rapid compared to thymus and spleen.
  • Kupffer cells play a significant role in clearing T-2 toxin-induced apoptotic cells in the liver.

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