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Nutrient Interactions and Toxicity

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© 2002 The American Society for Nutritional Sciences J. Nutr. 132:2723-2731,

September 2002

www.nutrition.org

Nutrient Interactions and Toxicity

The Mycotoxin Deoxynivalenol Affects Nutrient Absorption in Human Intestinal

Epithelial Cells1

Marc Maresca, Radhia Mahfoud, Nicolas Garmy and Jacques Fantini2

Institut Méditerranéen de Recherche en Nutrition, Unité Mixte de

Recherche-Institut National de la Recherche Agronomique, Faculté des

Sciences de Saint-Jérôme, Marseille, France

correspondence should be addressed. E-mail: jacques.fantini@....

Deoxynivalenol (DON) is a mycotoxin belonging to the tricothecene family

that has many toxic effects in animals, including diarrhea and weight loss.

Using the human epithelial intestinal cell line HT-29-D4 as an in vitro

model, we studied the effect of DON on the uptake of different classes of

nutrients, including sugars, amino acids and lipids. At low concentrations

(below 10 µmol/L), DON selectively modulated the activities of intestinal

transporters: the D-glucose/D-galactose sodium-dependent transporter (SGLT1)

was strongly inhibited by the mycotoxin (50% inhibition at 10 µmol DON, P <

0.05), followed by the D-fructose transporter GLUT5 (42% inhibition at 10

µmol/L, P < 0.001), active and passive L-serine transporters (30 and 38%

inhibition, respectively, at 10 µmol/L, P < 0.05). The passive transporters

of D-glucose (GLUT) were slightly inhibited by DON (15% inhibition at 1

µmol/L, P < 0.01), whereas the transport of palmitate was increased by 35%

at 10 µmol/L DON (P < 0.001). In contrast, the uptake of cholesterol was not

affected by the mycotoxin. At high concentrations (100 µmol/L), SGLT1

activity was inhibited by 76% (P < 0.01), whereas the activities of all

other transporters were increased. The selective effects of DON on

intestinal transporters were mimicked by cycloheximide and deoxycholate,

suggesting that inhibition of protein synthesis and induction of apoptosis

are the main mechanisms of DON toxicity in intestinal cells.

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