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Effet chez le porcelet d'une exposition à un régime co-contaminé en ...

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TRAVAIL EXPERIMENTALINTRODUCTIONMy<strong>co</strong>toxins are se<strong>co</strong>ndary metabolites of various f<strong>un</strong>gi <strong>co</strong>mmonly fo<strong>un</strong>d in feed and foodstuffs.Based on their known and suspected effects on human and animal health, aflatoxin, fumonisin,deoxyniva<strong>le</strong>nol, ochratoxin A and zeara<strong>le</strong>none are re<strong>co</strong>gnized as the five most important agriculturalmy<strong>co</strong>toxins (Shephard, 2008). The toxic effects of Fusarium my<strong>co</strong>toxins in animals include reducedgrowth, feed refusal, imm<strong>un</strong>osupression, gastrointestinal <strong>le</strong>sions, and neurological and reproductivedisorders (Rocha et al., 2005).Rec<strong>en</strong>t surveys demonstrated regular occurr<strong>en</strong>ce of low <strong>le</strong>vels of multip<strong>le</strong> my<strong>co</strong>toxins in cereals(Ros<strong>co</strong>e et al., 2008; Tabuc et al., 2009; Scudamore and Patel, 2009). Also, my<strong>co</strong>toxins may bepres<strong>en</strong>t in grains in <strong>co</strong>njugated chemical forms that escape detection through <strong>co</strong>nv<strong>en</strong>tional analyticalmethods (Zhou et al., 2007), resulting in an <strong>un</strong>derestimation of the total amo<strong>un</strong>t of my<strong>co</strong>toxins andfeed toxicity. Fusarium my<strong>co</strong>toxins in <strong>co</strong>mbination can exert more prono<strong>un</strong>ced effects in animalsthan individual my<strong>co</strong>toxins (Smith et al., 1997; Gr<strong>en</strong>ier et al., 2011).The intestinal tract is the first barrier against ingested antig<strong>en</strong>s, including my<strong>co</strong>toxins andpathog<strong>en</strong>ic bacteria. Following ingestion of my<strong>co</strong>toxin-<strong>co</strong>ntaminated food, <strong>en</strong>terocytes may beexposed to high <strong>co</strong>nc<strong>en</strong>trations of toxins (Bouhet and Oswald, 2005). Studies focusing on theinflu<strong>en</strong>ce of food-derived antig<strong>en</strong>s on intestinal morphology as an indicator of animal health are<strong>co</strong>mmon; meanwhi<strong>le</strong>, there are few publications on the effects of chronic exposure to a my<strong>co</strong>toxin<strong>co</strong>-<strong>co</strong>ntaminated diet.Fumonisins (FB) are toxic and carcinog<strong>en</strong>ic my<strong>co</strong>toxins produced by Fusarium verticillioides, a<strong>co</strong>mmon <strong>co</strong>ntaminant of maize. Fumonisin B1 (FB1) causes porcine pulmonary edema and equine<strong>le</strong>uko<strong>en</strong>cephalamalacia. An association betwe<strong>en</strong> human esophageal cancer and FB1 exposure indeveloping <strong>co</strong><strong>un</strong>tries has be<strong>en</strong> reported (Zhang et al., 1997). Fumonisins are structurally related tosphingoid bases and cause inhibition of ceramide synthase, <strong>le</strong>ading to accumulation of <strong>co</strong>rrespondingfree sphingoid bases, sphingoid base metabolites, and dep<strong>le</strong>tion of more <strong>co</strong>mp<strong>le</strong>x sphingolipids(Wang et al., 1991). In vitro, FB1 induces apoptosis, necrosis, and inhibition of proliferation in pigr<strong>en</strong>al epithelial (LLC-PK1) cells and human <strong>co</strong>lonic cells (HT29) (Gopee et al., 2003; Schmelz et al.,1998). FB1 can impair the intestinal absorption of nutri<strong>en</strong>ts. This can be explained by the villousfusion and atrophy observed in the intestines of pigs treated with 30 mg FB1/kg of feed and/or bysphingolipid disturbances (Taranu et al., 2005).Deoxyniva<strong>le</strong>nol (DON) causes toxic and imm<strong>un</strong>otoxic effects in a variety of cell systems andanimal species. DON is produced by F. graminearum and F. culmorum mainly in wheat, bar<strong>le</strong>y andmaize (Pestka and Smolinski, 2005). Swine is more s<strong>en</strong>sitive to DON than other species, in part110

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