Zebrafish (Danio rerio) as a model for investigating dietary toxic effects of deoxynivalenol contamination in aquaculture feeds
► This work presents dietary toxic effects of the mycotoxin, deoxynivalenol (DON) in zebrafish. ► It shows that zebrafish is not very sensitive to DON when it comes to fish performance. ► The work presents an evaluation of reproductive effects of DON. ► It shows that DON may affect the reproductive...
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Veröffentlicht in: | Food and chemical toxicology 2012-12, Vol.50 (12), p.4441-4448 |
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Sprache: | eng |
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Zusammenfassung: | ► This work presents dietary toxic effects of the mycotoxin, deoxynivalenol (DON) in zebrafish. ► It shows that zebrafish is not very sensitive to DON when it comes to fish performance. ► The work presents an evaluation of reproductive effects of DON. ► It shows that DON may affect the reproductive capability in a vertebrate animal.
The effects of feeding six diets spiked with increasing levels of DON for 45days to zebrafish (Danio rerio) on performance and liver gene biomarkers were investigated. In addition long term effects on fecundity, offspring larvae swimming activity and global DNA methylation in embryos were investigated. Zebrafish performance was not affected. Liver CYP1A mRNA levels were significantly higher in fish fed 2.0ppm DON compared to the control group, 0.1, 0.5 and 1.5ppm group. Gene transcripts of CuZn SOD and Cyclin G1 increased with increasing content of dietary DON. The percentage of 5-methylcytosine in embryos did not differ and was 7.0–7.1% across the groups. Fecundity showed a biphasic response pattern. Interestingly, fish fed 1.5ppm DON had 22% higher fecundity compared to control. A trend towards increased larvae swimming activity was seen in the high DON group. Our data suggest that DON is detoxified in the liver through the phase 1 system resulting in a disturbance in the oxidative balance. We do not know if effects observed on fecundity and larvae swimming activity are attributed to a direct interaction of DON with the reproductive organ or secondary to the maternal/paternal liver oxidative imbalance. |
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ISSN: | 0278-6915 1873-6351 |
DOI: | 10.1016/j.fct.2012.08.042 |