Cytotoxic Effects of Scirpene Compounds, Fusarenon-X Produced by Fusarium Nivale, Dihydronivalenol and Dihydrofusarenon-X, on Hela Cells

Ohtsubo, Kohichiro; Saitō, Mamoru

doi:10.7883/yoken1952.23.217

Cited by 16 publications

(9 citation statements)

References 13 publications

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“…The trichothecene mycotoxins, including nivalenol (NIV), which is produced by the Fusarium species, are highly cytotoxic to mammalian cells and act by inhibiting protein and DNA syntheses [6][7][8][9]. There has recently been a report of karyorrhexis observed in actively growing cells in bone marrow, thymus, and spleen of mice treated with these toxins [10].…”

Section: Introductionmentioning

confidence: 99%

The process of ultrastructural changes from nuclei to apoptotic body

et al. 1998

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There have been many reports on the formation of apoptotic bodies, but little is known about the cellular pathological processes and the morphological changes involved. We induced apoptotic cell death by administering nivalenol (NIV), a trichothecene mycotoxin produced by Fusarium species, and investigated the ultrastructural process of formation of apoptotic bodies. The thymus was examined by electron microscopy 6, 12, and 18 h after administration. Apoptotic cell death was induced in the thymus of NIV-treated mice. The nuclei became invaginated and pinched off to give fragments, and crescent-shaped spaces (CSS) were found around the nuclear envelopes of these cells at quite an early stage. In some of these spaces, myelin figures were observed. We divided the process of formation into four stages and characterized each of them. These are easily recognized in morphological stages and are also useful for clarifying the apoptotic mechanism.

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Section: Introductionmentioning

confidence: 99%

The process of ultrastructural changes from nuclei to apoptotic body

et al. 1998

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“…From numerous toxicologic studies in mice, rats, and cats, T-2 toxin was found to possess a potent activity to induce malfunction of hematopoietic organs, characterized by a marked decrease in numbers of circulating white blood cells [Sato et al, 1975[Sato et al, , 1978Ohtani et al, 1993], necrotic lesions and karyorrhexis of actively growing cells in bone marrow, thymus, and spleen [Saito and Ohtsubo, 1974], and impairment of immunologic responses [Masuko et al, 1977; for review, see Ueno, 1988]. Biochemical studies clarified that T-2 toxin and related trichothecenes exhibit a potent cytotoxicity toward mammalian cells by inhibiting protein synthesis [Ohtsubo and Saito, 1972;Ueno et al, 1973;Terse et al, 1993].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1997

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By 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.

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“…Skin irritation was also demonstrated (12). Biochemically, trichothecenes are a potent inhibitor of protein and DNA syntheses in rabbit reticulocytes, rat liver and other animal cells (11,(13)(14)(15)(16) MATERIALS AND METHODS Crude and pure samples of T-2 toxin were isolated from the culture filtrate of F. solani according to the method previously reported (7). The crude sample contained 4 % T-2 toxin and 1 % neosolaniol.…”

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Toxicological Approaches to the Toxic Metabolites of Fusaria

Sato

Ueno

Enomoto

1975

Japanese Journal of Pharmacology

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Abstract-Acuteand subacute toxicities to cats of T-2 toxin, 12-13 epoxytrichothec mycotoxin from fungi Fusarium species and others, were investigated. Major symp toms of toxicity in cats as the result of T-2 toxin were emesis, vomiting, diarrhea, anorexia, ataxia of the hind legs, discharge from the eyes and ejection of hemorrhagic fluid. Consecutive administration of the crude and pure sample of T-2 toxin in a sublethal dose caused a marked decrease in the number of circulating white blood cells. In the early stage of intoxication, a temporal leukocytosis was observed after each administration.Autopsy revealed extensive cellular damages in the bone mar row, intestine, spleen and lymph nodes. Greatly evident were meningeal hemorrhage of the brain, bleeding in the lungs and vacuolic degeneration of the renal tubles. Myco toxicological significance of T-2 toxin and related trichothecenes is discussed in rela tion to the food-borne diseases in humans and farm animals.

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Cytotoxic Effects of Scirpene Compounds, Fusarenon-X Produced by Fusarium Nivale, Dihydronivalenol and Dihydrofusarenon-X, on Hela Cells

Cited by 16 publications

References 13 publications

The process of ultrastructural changes from nuclei to apoptotic body

The process of ultrastructural changes from nuclei to apoptotic body

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

Toxicological Approaches to the Toxic Metabolites of Fusaria

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