T-2 Toxin-Induced Morphological Changes in Pregnant Rats

Sehata, Shinya; Teranishi, Munehiro; Atsumi, Fusako; Uetsuka, Koji; Nakayama, Hiroyuki; Doi, Kunio

doi:10.1293/tox.16.59

Cited by 12 publications

(10 citation statements)

References 21 publications

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“…An increase of single cell necrosis in the central nervous system of foetuses was observed at 24 hours after treatment. At 48 hours after treatment single cell necrosis of haematopoietic cells and hepatocytes was increased in the liver (Sehata et al, 2003).…”

Section: Developmental and Reproductive Toxicitymentioning

confidence: 98%

Report on toxicity data on trichothecene mycotoxins HT‐2 and T‐2 toxins

Schuhmacher-Wolz

Heine

Schneider

2010

EFSA Supporting Publications

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Section: Developmental and Reproductive Toxicitymentioning

confidence: 98%

Report on toxicity data on trichothecene mycotoxins HT‐2 and T‐2 toxins

Schuhmacher-Wolz

Heine

Schneider

2010

EFSA Supporting Publications

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“…The reproductive toxicity of T-2 toxin was also studied by Sehata et al (2003Sehata et al ( , 2004aSehata et al ( ,b, 2005. Pregnant Wistar rats were treated orally with T-2 toxin at a dose of 2 mg/kg b.w.…”

Section: Developmental and Reproductive Toxicitymentioning

confidence: 99%

“…As described in Section 7.3.7. above, Ishigami et al (1999Ishigami et al ( , 2001 and Sehata et al (2003Sehata et al ( , 2004b carried out studies on pregnant mice and rats exposed orally to T-2 toxin 2-3 mg/kg b.w., which showed apoptotic effects in the fetal brain.…”

Section: Neurotoxicitymentioning

confidence: 99%

Scientific Opinion on the risks for animal and public health related to the presence of T-2 and HT-2 toxin in food and feed

2011

EFSA Journal

281

102

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T-2 toxin and HT-2 toxin are mycotoxins produced by various Fusarium species. The European Commission asked EFSA for a scientific opinion on the risk to human and animal health related to the presence of T-2 and HT-2 toxin in food and feed. A total of 20,519 results for the sum of T-2 and HT-2 toxins in food, feed and unprocessed grains, collected in 2005-2010 from 22 European countries, were used in the evaluation. The highest mean concentrations for the sum of T-2 and HT-2 toxins were observed in grains and grain milling products, notably in oats and oat products. Grains and grain-based foods, in particular bread, fine bakery wares, grain milling products, and breakfast cereals, made the largest contribution to the sum of T-2 and HT-2 toxin exposure for humans. T-2 toxin is rapidly metabolised to a large number of products, HT-2 toxin being a major metabolite. Pigs are amongst the most sensitive animals towards the effects of T-2 toxin, the most sensitive endpoints being immunological or haematological effects. Using these data and a benchmark dose analysis the Panel on Contaminants in the Food Chain established a group tolerable daily intake (TDI) of 100 ng/kg b.w. for the sum of T-2 and HT-2 toxins. Estimates of chronic human dietary exposure to the sum of T-2 and HT-2 toxins based on the available occurrence data are below the TDI for populations of all age groups, and thus not a health concern. For ruminants, rabbits and farmed fish the estimated exposures to the sum of these toxins based on the available occurrence data are considered unlikely to be a health concern, while for pigs, poultry, dogs and horses the risk of adverse health effects is low. For cats the health risk from the exposure to T-2 and HT-2 toxins cannot be assessed.

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“…Sehata et al . [ 41 , 42 ] examined the maternal toxicity in detail in pregnant rats exposed to a single oral dose of T-2 toxin (2 mg/kg) on day 13 of gestation. In their experiments, apoptosis was induced in lymphoid, hematopoietic and gastrointestinal tissues and liver as described in the above-mentioned reports in adult mice.…”

Section: Maternal Toxicitymentioning

confidence: 99%

T-2 Toxin-induced Toxicity in Pregnant Mice and Rats

Doi

Ishigami

Sehata

2008

IJMS

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T-2 toxin is a cytotoxic secondary fungal metabolite that belongs to the trichothecene mycotoxin family. This mycotoxin is a well known inhibitor of protein synthesis through its high binding affinity to peptidyl transferase, which is an integral part of the ribosomal 60s subunit, and it also inhibits the synthesis of DNA and RNA, probably secondary to the inhibition of protein synthesis. In addition, T-2 toxin is said to induce apoptosis in many types of cells bearing high proliferating activity. T-2 toxin readily passes the placenta and is distributed to embryo/fetal tissues, which include many component cells bearing high proliferating activity. This paper reviews the reported data related to T-2 toxin-induced maternal and fetal toxicities in pregnant mice and rats. The mechanisms of T-2 toxin-induced apoptosis in maternal and fetal tissues are also discussed in this paper.

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T-2 Toxin-Induced Morphological Changes in Pregnant Rats

Cited by 12 publications

References 21 publications

Report on toxicity data on trichothecene mycotoxins HT‐2 and T‐2 toxins

Report on toxicity data on trichothecene mycotoxins HT‐2 and T‐2 toxins

Scientific Opinion on the risks for animal and public health related to the presence of T-2 and HT-2 toxin in food and feed

T-2 Toxin-induced Toxicity in Pregnant Mice and Rats

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