Ameliorative effects of Bacillus subtilis ANSB01G on zearalenone toxicosis in pre-pubertal female gilts

The purpose of this research was to investigate the toxicity of zearalenone (ZEA) on the growing performance, genital organs, serum hormones and histopathological changes of pre-pubertal female gilts, and to evaluate the efficacy of Bacillus subtilis ANSB01G in alleviating ZEA toxicosis in gilts. Eighteen pre-pubertal female gilts were randomly allocated to three treatments with one replicate per treatment. The gilts were fed following three diets for 24 days: the Control group was given a basic diet with normal corn; Treatment 1 (T1) was prepared by substituting corn naturally contaminated with ZEA for all normal corn in the basic diet (with a final concentrations of 238.57 μg kg ⁻¹ of ZEA); and Treatment 2 (T2) was prepared by mixing the T1 diet with 2 kg T ⁻¹ of fermented–dried culture of ANSB01G. The results showed that the presence of ZEA in diets significantly increased the vulva size and reproductive organ weight of the T1 gilts as compared with the Control group, and the addition of ANSB01G to diet naturally contaminated with ZEA obviously ameliorated these symptoms, as was observed in the T2 group. The presence of low doses of ZEA in the T1 diet had no significant effect on the level of follicle-stimulating hormone (FSH), luteotrophic hormone (LH) or serum oestradiol (E2) in the serum of gilts, but the prolactin (PRL) level in group T1 increased significantly. The gilts of the T1 group exhibited conspicuous cell enlargement and fatty degeneration of the corpus uteri, swelling, inflammation and lymphocyte infiltration of liver cells as compared with the Control group. The presence of ANSB01G can alleviate these hyperoestrogenic effects caused by ZEA, maintaining the body of gilt in a normal and healthy status. It is suggested that reproductive organs of gilts are seriously affected even if they are fed a low dose of ZEA in less time, and the addition of B. subtilis ANSB01G can effectively alleviate ZEA toxicosis in gilts.