Effect of zearalenone on aflatoxin B1-induced intestinal and ovarian toxicity in pregnant and lactating rats

Aflatoxin B1 (AFB1) and zearalenone (ZEN) cause serious damage to mammals, but few studies have investigated the impacts of these toxins on pregnant and lactating mammals. This study investigated the effects of ZEN on AFB1-induced intestinal and ovarian toxicity in pregnant and lactating rats. Based on the results, AFB1 reduces the digestion, absorption, and antioxidant capacity in the intestine, increases intestinal mucosal permeability, destroys intestinal mechanical barriers, and increases pathogenic bacteria' relative abundances. Simultaneously, ZEN can exacerbate the intestinal injury caused by AFB1. The intestines of the offspring were also damaged, but the damage was less severe than that observed for the dams. While AFB1 activates various signalling pathways in the ovary and affects genes related to endoplasmic reticulum stress, apoptosis, and inflammation, ZEN may exacerbate or antagonize the AFB1 toxicity on gene expression in the ovary through key node genes and abnormally expressed genes. Our study found that mycotoxins can not only directly damage the ovaries and affect gene expression in the ovaries but can also impact ovarian health by disrupting intestinal microbes. Mycotoxins are an important environmental pathogenic factor for intestinal and ovarian disease in pregnancy and lactation mammals.

Automated summary

This study investigated the effects of Aflatoxin B1 (AFB1) and zearalenone (ZEN) on the intestines and ovaries of pregnant and lactating rats. The results showed that AFB1 reduces digestion, absorption, and antioxidant capacity in the intestines, increases intestinal mucosal permeability, and disrupts the intestinal microbiota. ZEN exacerbates the intestinal injury caused by AFB1. Additionally, AFB1 affects ovarian genes and signaling pathways, while ZEN may either exacerbate or counteract AFB1's toxicity on ovarian gene expression. This study highlights the importance of mycotoxins in the development of intestinal and ovarian diseases in pregnant and lactating mammals.