Effect of 4-week feeding of deoxynivalenol- or T-2-toxin-contaminated diet on lipid peroxidation and glutathione redox system in the hepatopancreas of common carp (Cyprinus carpio L.)

Abstract

The purpose of study was to investigate the effects of T-2 toxin (4.11 mg T-2 toxin and 0.45 mg HT-2 toxin kg(-1) feed) and deoxynivalenol (5.96 and 0.33 mg 15-acetyl deoxynivalenol (DON) kg(-1) feed) in 1-year-old common carp juveniles in a 4-week feeding trial. The exposure of mycotoxins resulted in increased mortality in both groups consuming mycotoxin-contaminated diet. Parameters of lipid peroxidation were not affected during the trial, and antioxidant defence also did not show response to oxidative stress; however, glutatione peroxidase activity slightly, but significantly, decreased in the T-2 toxin group. Glutathione S-transferase activity showed moderate decrease as effect of T-2 toxin, which suggests its effect on xenobiotic transformation. Reduced glutathione concentration showed moderate changes as effect of DON exposure, but T-2 toxin has no effect. Expression of phospholipid hydroperoxide glutathione peroxidase (GPx4) genes showed different response to mycotoxin exposure. T-2 toxin caused dual response in the expression of gpx4a (early and late downregulation and mid-term upregulation), but continuous upregulation was found as effect of deoxynivalenol. Expression of the other gene, gpx4b, was upregulated by both trichothecenes during the whole period. The results suggested that trichothecenes have some effect on free radical formation and antioxidant defence, but the changes depend on the duration of exposure and the dose applied, and in case of glutathione peroxidase, there was no correlation between expression of genes and enzyme activity.

Short-term effects of T-2 toxin or deoxynivalenol on lipid peroxidation and the glutathione system in common carp

“…In that trial, the parameters of lipid peroxidation did not differ, therefore they did not show oxidative stress; however, GPx activity decreased in the group challenged with T-2 toxin. The expression of GPx genes was continuously overregulated by DON exposure in that long-term trial, while T-2 toxin had no such effect (Pelyhe et al, 2016). The differences between gene expression and activity at the same time can be explained by the post-translational modification of GPx, which enhanced activity (Fritz et al, 2012).…”

“…In a long-term feeding trial with common carp, T-2 toxin resulted in an elevated level of reduced glutathione and affected glutathione peroxidase activity, without increasing the terminal marker of lipid peroxidation, thiobarbituric reactive substances (Balogh et al, 2009). A recent long-term study on common carp with a high dietary inclusion of T-2 and HT-2 toxins or DON and 15-acetyl DON also revealed that the oxidative stress parameters did not differ significantly; however, the expression of phospholipid hydroperoxide glutathione peroxidase genes (gpx4a and gpx4b) showed some, but not conclusive, differences attributable to the effect of T-2 or DON (Pelyhe et al, 2016).…”

Influence of mycotoxins on fish health

“…U ssaków mikotoksyna T-2 może indukować apoptozę komórek poprzez uszkodzenie DNA wywoływane powstaniem stresu oksydacyjnego lub upośledzoną syntezą białek (25). Rola stresu oksydacyjnego i jego występowanie zostały wykazane wśród karpi narażonych na doustne podanie deoksyniwalenolu (33), jednakże w badaniach prowadzonych na narybku karpia nie wykazano zdolności trichotecenów do wzbudzania stresu oksydacyjnego, pomimo zaobserwowania zwiększonej śmiertelności wśród badanych grup ryb (25). Różne odpowiedzi organizmu ryb na te same patogeny niektórzy autorzy przypisują obecności flory mikrobiologicznej, która posiada zdolność do metabolizowania mikotoksyn w przewodzie pokarmowym (25).…”

“…Rola stresu oksydacyjnego i jego występowanie zostały wykazane wśród karpi narażonych na doustne podanie deoksyniwalenolu (33), jednakże w badaniach prowadzonych na narybku karpia nie wykazano zdolności trichotecenów do wzbudzania stresu oksydacyjnego, pomimo zaobserwowania zwiększonej śmiertelności wśród badanych grup ryb (25). Różne odpowiedzi organizmu ryb na te same patogeny niektórzy autorzy przypisują obecności flory mikrobiologicznej, która posiada zdolność do metabolizowania mikotoksyn w przewodzie pokarmowym (25). Dowiedziono, że niektóre gatunki bakterii z rodzaju Bacillus dzięki właściwościom enzymatycznym -wytwarzanie chitynazy, glukanazy i proteinazy -mają zdolność hamowania wzrostu grzybów (37).…”

Combined effects of aflatoxin B1 and deoxynivalenol on the expression of glutathione redox system regulatory genes in common carp

“…Šišperová et al (2015) observed that DON causes oxidative stress in rainbow trout and it has also been reported that AFB 1 induces the formation of reactive oxygen species, which may cause oxidative stress (Shen, Shi, Shen, & Ong, 1996). Both AFB 1 -and DON-induced oxidative stress affect the enzymatic and non-enzymatic antioxidant defences and alter the transcription factor nuclear factor-erythroid 2 p45-related factor 2 (Nrf2), which is the key regulator of the oxidative stress response, and its main negative regulator Kelch-like ECH-associated protein 1 (KEAP1) gene expression (Kövesi, Pelyhe, Zándoki, Mézes, & Balogh, 2018;Pelyhe et al, 2016aPelyhe et al, , 2016b. Under basal conditions, Keap1 binds Nrf2 and recruits it into the Cul3containing E3 ubiquitin ligase complex for ubiquitin conjugation and proteasomal degradation (Motohashi & Yamamoto, 2004).…”