Vomitoxin (4-deoxynivalenol): effects on reproduction of mice and rats

Khera, K. S.; Arnold, Douglas L.; Whalen, C.; Angers, G.; Scott, Peter

doi:10.1016/0041-008x(84)90288-6

Cited by 49 publications

(29 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T-2 reduced body weight gain in pigs (Weaver et al 1978) and DON and NIV caused growth retardation in mice (Ryu et al 1988, Ohtsubo et al 1989. Reproductive defects in mice caused by trichothecenes include embryo or foetal toxicity caused by T-2 toxin (Rousseaux et al 1986), increased postnatal mortality caused by DON (Khera et al 1984) and intrauterine growth retardation caused by NIV (Ito et al 1988). DON increased the susceptibility of mice to infections (Tryphonas et al 1986).…”

Section: Gross Toxic Effects Of Trichothecenes On Animalsmentioning

confidence: 99%

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Rocha

Ansari²,

Doohan³

2005

Food Additives and Contaminants

493

298

View full text Add to dashboard Cite

The major products of the trichothecene mycotoxin biosynthetic pathway produced in a species-and sometimes isolatespecific manner by cereal-pathogenic Fusarium fungi include T-2 toxin, diacetoxyscirpenol, deoxynivalenol and nivalenol. This paper briefly reviews the major effects of such trichothecenes on the gross morphology, cytology and molecular signalling within eukaryotic cells. The gross toxic effects of select trichothecenes on animals include growth retardation, reduced ovarian function and reproductive disorders, immuno-compromization, feed refusal and vomiting. The phytotoxic effects of deoxynivalenol on plants can be summarized as growth retardation, inhibition of seedling and green plant regeneration. Trichothecenes are now recognized as having multiple inhibitory effects on eukaryote cells, including inhibition of protein, DNA and RNA synthesis, inhibition of mitochondrial function, effects on cell division and membrane effects. In animal cells, they induce apoptosis, a programmed cell death response. Current knowledge about the eukaryotic signal transduction cascades and downstream gene products activated by trichothecenes is limited, especially in plants. In mammalian cells, certain trichothecenes trigger a ribotoxic stress response and activate mitogen-activated protein kinases. DON mediates the inflammatory response by modulating the binding activities of specific transcription factors and subsequently inducing cytokine gene expression. Several genes are up-regulated in wheat in response to trichothecene mycotoxins; the significance, if any, of these genes in the host response to trichothecenes has yet to be elucidated.

show abstract

Section: Gross Toxic Effects Of Trichothecenes On Animalsmentioning

confidence: 99%

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Rocha

Ansari²,

Doohan³

2005

Food Additives and Contaminants

493

298

View full text Add to dashboard Cite

show abstract

“…Khera et al [6] have described a high level of resorption, and severe abnormalities in the rare surviving foetuses after doses of 10-15 µg/g of DON were given to pregnant mice. Bergsjo et al [2] have shown that DON may induce delayed ossification in the chick.…”

Section: Introductionmentioning

confidence: 99%

Skeletal deformities induced by the intraperitoneal administration of deoxynivalenol (vomitoxin) in mice

Debouck¹,

Haubruge

Bollaerts

et al. 2001

International Orthopaedics (SICOT)

View full text Add to dashboard Cite

The contamination of drinking water by organic acids, selenium deficiency and the ingestion of fungal mycotoxins are the three main aetiological factors in the development of Kashin-Beck disease. An avian tibial chondrodysplasia induced by mycotoxins has been reported. Deoxynivalenol (DON) is one of many mycotoxins produced by the most common contaminating species of fungi. The pattern of skeletal malformations induced by its administration intraperitoneally to pregnant mice is reported. Costo-vertebral segmentation abnormalities were the main deformities observed. The chondrodysplasia previously described was not seen. Résumé La contamination de l'eau potable par des acides organiques, une déficience en sélénium et une intoxication par des mycotoxines sont les trois principaux facteurs etiopathogéniques proposés dans la maladie de Kashin-Beck. Une chondrodysplasie tibiale a été décrite chez l'Oiseau. Elle était provoquée par des mycotoxines. Le désoxynivalenol (DON) est une mycotoxine communément produite par divers taxons de champignons qui contaminent les céréales et la nourriture. L'administration intrapéritonéale de DON à la souris gestante a provoqué des malformations squelettiques diverses. Les anomalies de segmentation costo-vertébrales sont les plus fréquentes dans le cadre du schéma choisi d'administration de la drogue. Nous n'avons pas pu reproduire dans cette étude préliminaire un syndrome de chondrodysplasie tibiale analogue à celui décrit chez l'Oiseau.

show abstract

“…In Swiss-Webster mice, Khera et al (1982;1984) observed a high incidence of embryonic resorption, reduced foetal weight and an increased incidence of skeletal and visceral malformations. In rats, reproduction toxicity of DON has been demonstrated by Khera et al (1984), Morrisey (1984), and Morrisey and Vesonder (1985), either as reduced fertility, decreased foetal body weight, or minor foetal malformations. Embryo-toxicity following administration of DON to rabbits was reported by Khera et al (1986).…”

Section: Discussionmentioning

confidence: 96%

Effects of feeding deoxynivalenol‐contaminated oats on reproduction performance in white leghorn hens

Bergsj

Herstad

Nafstad

1993

British Poultry Science

View full text Add to dashboard Cite

1. The effect of feeding trichothecene-contaminated diets with graded concentrations of deoxynivalenol ranging from 120 to 4900 micrograms/kg to groups of laying hens was investigated. 2. Food intake, weight gain and egg production were not affected by mycotoxin administration. No significant differences were found between groups. 3. The overall results from the hatching tests did not reveal any significant differences in fertility, hatchability or perinatal mortality, which could be explained by the mycotoxin content in the diets. 4. Body weight at hatching and viability of the chicks were not affected by the mycotoxin concentrations in the diets. 5. The incidence of chick developmental anomalies was increased in the mycotoxin-administered groups compared to controls. Minor malformations were the dominating anomalies and included unwithdrawn yolk sac and delayed ossification. The most frequent major malformations were cloacal atresia and cardiac anomalies.

show abstract

Vomitoxin (4-deoxynivalenol): effects on reproduction of mice and rats

Cited by 49 publications

References 5 publications

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Effects of trichothecene mycotoxins on eukaryotic cells: A review

Skeletal deformities induced by the intraperitoneal administration of deoxynivalenol (vomitoxin) in mice

Effects of feeding deoxynivalenol‐contaminated oats on reproduction performance in white leghorn hens

Contact Info

Product

Resources

About