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

Wiley - Tập 5 Số 4 - Trang 141-145 - 1997
Tomomi Ihara1, Masao Sugamata1, Masaru Sekijima2, Hiroki Okumura3, Naoto Yoshino3, Yoshio Ueno3
1Department of Pathology, Institute of Tochigi Clinical Pathology, Tochigi, Japan
2Kashima Laboratory, Mitsubishi Chemical Safety Institute, Ibaraki, Japan
3Department of Toxicology and Microbial Chemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Ichigaya, Tokyo, Japan

Tóm tắt

AbstractBy histopathologic, electron microscopic, and immunochemical observation, the mechanism of cellular death was investigated in thymus, spleen, and liver of mice given intraperitoneally sublethal doses of T‐2 toxin, a trichothecene mycotoxin. In the thymus and spleen of mice given 5.0 mg/kg body weight of T‐2 toxin and killed 12 hours later, a massive cellular destruction characterized by chromatin condensation was evident, and electron microscopy analysis revealed the presence of apoptotic bodies. In the liver of mice given 2.5 mg/kg of T‐2 toxin and killed 2 hours later, the induction of apoptotic cellular lesions was observed by electron microscopy, and Kupffer cells phagocytosed the apoptotic bodies. Such lesions were not observed in the mice killed 12 hours after receiving the toxin. In situ nick translation analysis (Tunel method) revealed DNA fragmentation in thymus, spleen, and liver shortly after administration of T‐2 toxin. As previously observed in vitro, these findings indicated that T‐2 toxin is a potent inducer of apoptotic cell death in thymus, spleen, and liver in vivo; especially in liver, apoptosis is induced rapidly as compared with the other tissues observed, and Kupffer cells play an important role for clearance of apoptosis. Nat. Toxins 5:141–145, 1997. © 1997 Wiley‐Liss, Inc.

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Wiley

Tập 5 Số 4

141-145

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