Deoxynivalenol (DON) and fumonisins (FB) are mycotoxins produced byFusariumspecies, which naturally co-occur in animal diets. The gastrointestinal tract represents the first barrier met by exogenous food/feed compounds. The purpose of the present study was to investigate the effects of DON and FB, alone and in combination, on some intestinal parameters, including morphology, histology, expression of cytokines and junction proteins. A total of twenty-four 5-week-old piglets were randomly assigned to four different groups, receiving separate diets for 5 weeks: a control diet; a diet contaminated with either DON (3 mg/kg) or FB (6 mg/kg); or both toxins. Chronic ingestion of these contaminated diets induced morphological and histological changes, as shown by the atrophy and fusion of villi, the decreased villi height and cell proliferation in the jejunum, and by the reduced number of goblet cells and lymphocytes. At the end of the experiment, the expression levels of several cytokines were measured by RT-PCR and some of them (TNF-α, IL-1β, IFN-γ, IL-6 and IL-10) were significantly up-regulated in the ileum or the jejunum. In addition, the ingestion of contaminated diets reduced the expression of the adherent junction protein E-cadherin and the tight junction protein occludin in the intestine. When animals were fed with a co-contaminated diet (DON+FB), several types of interactions were observed depending on the parameters and segments assessed: synergistic (immune cells); additive (cytokines and junction protein expression); less than additive (histological lesions and cytokine expression); antagonistic (immune cells and cytokine expression). Taken together, the present data provide strong evidence that chronic ingestion of low doses of mycotoxins alters the intestine, and thus may predispose animals to infections by enteric pathogens.

Mycotoxins are the most common contaminants of food and feed worldwide and are considered an important risk factor for human and animal health. Oxidative stress occurs in cells when the concentration of reactive oxygen species exceeds the cell’s antioxidant capacity. Oxidative stress causes DNA damage, enhances lipid peroxidation, protein damage and cell death. This review addresses the toxicity of the major mycotoxins, especially aflatoxin B₁, deoxynivalenol, nivalenol, T-2 toxin, fumonisin B₁, ochratoxin, patulin and zearalenone, in relation to oxidative stress. It summarises the data associated with oxidative stress as a plausible mechanism for mycotoxin-induced toxicity. Given the contamination caused by mycotoxins worldwide, the protective effects of a variety of natural compounds due to their antioxidant capacities have been evaluated. We review data on the ability of vitamins, flavonoids, crocin, curcumin, green tea, lycopene, phytic acid, L-carnitine, melatonin, minerals and mixtures of anti-oxidants to mitigate the toxic effect of mycotoxins associated with oxidative stress.