Fusarium head blight (FHB), mainly caused by Fusarium graminearum and F. culmorum, is a worldwide disease of wheat (Triticum aestivum L.), resulting in significant loss in both yield and quality. Use of resistant cultivars is an effective strategy for managing FHB and reducing mycotoxin production in wheat. Understanding of the histochemical, physiological, biochemical and molecular mechanisms involved in FHB resistant and susceptible wheat cultivars is limited so far. In this research, we investigated the role of reactive oxygen species (ROS), non-enzymatic and enzymatic antioxidants in basal resistance of wheat to the hemibiotrophic and necrotrophic Fusarium species causing FHB. Gaskozhen and Falat plants were used as partially resistant and susceptible wheat cultivars against Fusarium spp., respectively. Accumulation of H2O2 and O2 − was higher in Gaskozhen compared to Falat cultivar. The obtained results revealed considerably higher levels of non-enzymatic and enzymatic antioxidants after inoculation with Fusarium spp. in Gaskozhen compared to Falat cultivar at most of the time points investigated. No significant increase in the accumulation and activity of various antioxidants was observed in the uninoculated control plants in most cases during the time period tested. Significantly higher disease progress in the leaves of both cultivars treated with KCN, as an inhibitor of not only GPOX but also CuZnSOD and MnSOD, revealed the major role of these antioxidantive enzymes compared to FeSOD, APX and CAT in wheat defense responses to Fusarium species. Expression analysis of the genes responsible for production of enzymatic antioxidants using RT-PCR revealed a direct correlation between enzyme activities and expression of the corresponding genes. Application of ROS generating systems increased disease progress in both cultivars. Investigating wheat-Fusarium spp. interaction showed that F. culmorum isolate induced higher levels of ROS and antioxidants compared to F. graminearum. In addition, application of enzymatic antioxidant inhibitors reduced H2O2 and O2− levels, which led to increased disease development.

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