Abstract
BackgroundT-2 toxin is a mycotoxin produced by Fusarium species that is highly toxic to animals. Recent studies have indicated that Selenomethionine (SeMet) have protective effect against mycotoxins-induced toxicity. The aim of the present study was to investigate the protective effect of SeMet on T-2-toxin-induced liver injury in rabbit and explore its molecular mechanism. Fifty rabbits (30 d, 0.5 ± 0.1 kg) were randomly divided into 5 groups: control group, T-2 toxin group, low, medium and high dose SeMet treatment group. The SeMet-treated group was orally pretreated with SeMet (containing selenium 0.2 mg/kg, 0.4 mg/kg and 0.6 mg/kg) for 21 days. On the 17th day, T-2 toxin group and SeMet-treated group were orally administered with T-2 toxin (0.4 mg/kg body weight) for 5 consecutive days.ResultsThe results showed that low-dose SeMet significantly improved T-2 toxin-induced liver injury. We found that low-dose SeMet can reduce the level of oxidative stress and the number of hepatocyte apoptosis. Moreover, the levels of Bax, caspase-3 and caspase-9 were significantly reduced and the levels of Bcl-2 were increased.ConclusionsTherefore, we confirmed that low-dose SeMet may protect rabbit hepatocytes from T-2 toxin by inhibiting the mitochondrial-caspase apoptosis pathway.
Highlights
T-2 toxin is a mycotoxin produced by Fusarium species that is highly toxic to animals
In the low-dose and medium-dose SeMet+T-2 toxin group, we found that activities of AST, ALT, and Alkaline phosphatase (ALP) decreased to different degrees compared with the T-2 toxin group, and total protein (TP) levels increased in varying degrees (Fig. 1)
There was no difference between the T-2 toxin group and the high-dose SeMet group. These results indicate that SeMet at the low and medium doses can reduce the increase of Bcl-2-Associated X (Bax), Caspase-3, and Caspase-9 expression in liver cells induced by T-2 toxin, and increase B-cell lymphoma2 (Bcl-2) expression levels
Summary
T-2 toxin is a mycotoxin produced by Fusarium species that is highly toxic to animals. The aim of the present study was to investigate the protective effect of SeMet on T-2-toxin-induced liver injury in rabbit and explore its molecular mechanism. T-2 toxin is a secondary metabolite produced by different species of Fusarium including F. soprotrichioides, F. poae and F. acuinatum, which can infect corn, wheat, barley, rice and other crops in the field and in storage under tropical climate or humid storage conditions [1]. It has extremely high chemical stability under changing environmental conditions, so that autoclaving is not easy to inactivate T-2 toxins during feed production and processing. Oxidative stress [6] is characterized by downregulation of total antioxidant capacity (T-AOC) and
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