Abstract. The nutritional deficiencies provoked by ethanol consumption, during gestation or lactation, can contribute to multiple birth defects in offspring. In order to improve our knowledge about selenium (Se) distribution in pups exposed to ethanol, the present study evaluated the effect of this drug on intestinal development and determined its action on duodenal absorption of selenomethionine (Se-Met). To determinate if supplementation could improve Se absorption and its serum values, we used two antioxidant supplemented regimens on dams, with selenium alone or selenium plus folic acid, and obtained six groups of pups: C (control), A (alcohol), CS (control + Se), AS (alcohol + Se), CFS (control + Se + folic acid) and AFS (alcohol + Se + folic acid). Duodenal Se-Met transport was performed using an in vivo perfusion method. Se levels were measured by graphite furnace atomic absorption spectrometry. The supplemented diets utilized had a positive influence on body growth, duodenal perimeter and Se content in ethanol-exposed pups. Ethanol exposure increased Se-Met duodenal absorption in all pups, supplemented or not, presenting the highest values of maximal velocity (V max ) compared with their control counterparts. The affinity constant (K m ) increased according to rank: A>AS>AFS groups. These results suggest that although antioxidant supplementation does not restore Se-Met absorption to normal values, it enhances the affinity of the transporters for the substrate and improves the damage caused by ethanol in the duodenal mucosa.Key words: Ethanol, Kinetic parameters, Offspring development, Selenomethionine absorption (J. Reprod. Dev. 57: [708][709][710][711][712][713][714] 2011) T he primary function of the intestinal epithelium is to absorb the small molecules produced from food digestion [1]. However, specific substances such as alcohol could alter this intestinal absorption [2,3], producing malnutrition. Numerous studies have demonstrated that chronic ethanol consumption induces morphological and biochemical alterations in the intestinal mucosal cells [4] and that some of these changes are caused by a lipid peroxidation of duodenal membrane lipids [5]. These effects of ethanol exposure are more acute during pregnancy and lactation and can contribute to a delay in offspring growth and multiple birth defects, including fetal alcohol syndrome [6]. In this context, it is especially relevant that ethanol deregulates the homeostasis of different antioxidants such as folic acid, whose deficiency is the most common sign of malnutrition in chronic alcoholism [7]. This deficiency is associated with several alterations such as Down's syndrome and defects in neural tube closure in developing embryos [1]. According to what we have previously reported [8], the effects of ethanol exposure during gestation and lactation on folic acid intestinal absorption showed that intestinal folate absorption appears to be upregulated in suckling rats. Our research group has also found, in pups exposed to ethanol and supplemented wit...