# UDP-glycosyltransferases alleviate the toxic effects of deoxynivalenol on the growth performance and gut damage of Kunming mice

## TL;DR

This study shows that UDP-glycosyltransferases help reduce the harmful effects of deoxynivalenol on mice growth and gut health.

## Contribution

UGTs are shown to mitigate DON-induced gut damage and growth issues in Kunming mice.

## Key findings

- UGTs reduced DON and CTX-induced gut damage and improved growth performance in mice.
- UGTs improved antioxidant enzyme activity and intestinal barrier integrity in treated mice.
- UGTs decreased intestinal cell apoptosis and histopathological lesions in mice.

## Abstract

The purpose of this study was to assess the effects of UDP-glycosyltransferases (UGTs) on alleviating the toxic effects of deoxynivalenol (DON) on Kunming mouse growth performance and gut damage. In this study, a total of 60 3-week-old male Kunming mice were randomly divided into 4 groups and fed the following dietary and drug treatments for 7 weeks: CON, basal diet; CTX, basal diet with i.p. injection of cyclophosphamide (CTX); CTX + DON, basal diet with 12 mg/kg DON and i.p. injection of cyclophosphamide; and CTX + DON + UGTs, basal diet with 12 mg/kg DON and UGTs 1 mg/kg and i.p. injection of cyclophosphamide. Compared with those in the CON group, the growth performance, serum immunoglobulin contents (IgG), antioxidant defense enzyme activities(SOD), intestinal barrier integrity and permeability (the ratio of villi length to crypt depth), tight junction proteins (occludin and claudin 5) expression, intestinal cell apoptosis (Bcl-2), and histopathological lesions in the guts of the DON- and CTX-treated mice were significantly lower (p < 0.05). These negative effects on DON-exposed mice were significantly mitigated when the mice received a UGT-supplemented diet (1 mg/kg) (p < 0.05). We concluded that UGTs could serve as dietary supplements to treat intestinal disorders associated with DON-induced growth-retardation in animals.

The online version contains supplementary material available at 10.1038/s41598-025-02712-6.