Mycotoxins are toxic fungal metabolites, contaminating cereal grains in field or during processing and storage periods. These environmental contaminants pose great threats to humans and animals’ health due to their toxic effects. Type A trichothecenes, fumonisins and fusaric acid (FA) are commonly detected mycotoxins produced by various Fusarium species. Trichoderma spp. are promising antagonists in agriculture for their activities against plant pathogens, and also regarded as potential candidates for bioremediation of environmental contaminants. Managing toxigenic fungi by antagonistic Trichoderma is regarded as a sustainable and eco-friendly strategy for mycotoxin control. However, the metabolic activities of Trichoderma on natural occurring mycotoxins were less investigated. Our current work comprehensively explored the activities of Trichoderma against type A trichothecenes, fumonisins and FA producing Fusarium species via co-culture competition and indirect volatile assays. Furthermore, we investigated metabolism of type A trichothecenes and FA in Trichoderma isolates. Results indicated that Trichoderma were capable of bio-transforming T-2 toxin, HT-2 toxin, diacetoxyscirpenol and neosolaniol into their glycosylated forms and one Trichoderma strain could bio transform FA into low toxic fusarinol. These findings proved that Trichoderma isolates could manage toxigenic Fusarium via direct competition and volatile-mediated indirect inhibition. In addition, these antagonists possess defensive systems against mycotoxins for self-protection, which enriches our understanding on the interaction mechanism of Trichoderma spp. on toxigenic fungus.

HT-2 toxin (HT-2), a mycotoxin produced by Fusarium species, is detected in a variety of cereal grain-based human food and animal feed. Apart from its well-established immunotoxicity and haematotoxicity, it also causes reproductive disorders. In the present study, we revealed the adverse effects of HT-2 on early oogenesis at the foetal stage. Pregnant mice were orally administered with HT-2 for 3 days at mid-gestation. Oocytes from female foetuses exposed to HT-2 displayed defects in meiotic prophase, including unrepaired DNA damage, elevated recombination levels, and reduced expression of meiotic-related genes. Subsequently, increased oxidative stress was observed in the foetal ovaries exposed to HT-2, along with the elevated levels of reactive oxygen species, malondialdehyde, catalase, and superoxide dismutase 1/2, thereby resulting in impaired mitochondrial membrane potential and cell apoptosis. Furthermore, pre-treatment with urolithin A, a natural compound with antioxidant activities, partially reversed the delayed meiotic process by alleviating oxidative stress. Since early oogenesis is essential to determine female fertility in adult life, this study indicated that brief maternal exposure to HT-2 toxin may compromise the fertility of a developing female foetus.