Target 2 (T-CURX)

T‐2 toxin is a member of class A aspergilloides toxins, one of the most prevalent mycotoxins that contaminate feed and food. Direct ingestion of animals or feed contaminated by T‐2 toxin can cause various animal diseases. Butyrate is an organic fatty acid featuring a four‐carbon chain, which is commonly found in the form of sodium butyrate (NaB). NaB has several biological functions and pharmacological effects. However, the role of sodium butyrate in alleviating T‐2 toxin–induced hepatorenal toxicity has not been explored. In this study, 240 juvenile quails were evenly assigned into 4 groups. The experimental setup comprised four groups: The control group received a standard diet; the toxin group received a diet containing 0.9 mg/kg T‐2 toxin; the butyrate group received a diet containing 0.5 g/kg NaB; and the T‐2 treatment group received a diet containing both 0.9 mg/kg T‐2 toxin and 0.5 g/kg NaB. We evaluated the histopathological changes in the kidney and liver on Days 14 and 28 and explored the molecular mechanisms involving oxidative stress, inflammation, and expression of nuclear xenobiotic receptors (NXRs). Our results showed that T‐2 toxin exposure–induced inflammation in the liver and kidney by activating the oxidative stress pathway and modulating expression of NXRs to regulate related CYP450 isoforms, ultimately leading to histopathological injury in the liver and kidney, whereas sodium butyrate ameliorated this injury. These results offer novel insights into the molecular mechanisms underlying the protective effects of sodium butyrate in mitigating T‐2 toxin–induced hepatorenal injury in juvenile quails.

The mechanisms of T‐2 toxin toxicity have been well described in experimental animals, but studies in birds are limited. With the development of society, the market scale of quails farming has been expanding, and the value of quails meat and eggs is increasing; there is an urgent need to clarify the harm of T‐2 toxin to quails and its mechanism.