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Nutrient Interactions and Toxicity
Research Communication

The Antioxidant BHT Normalizes Some Oxidative Effects of Iron + Ascorbate on Lipid Metabolism in Caco-2 Cells¹

Frédéric Courtois^*, Edgard Delvin, Marielle Ledoux^*, Ernest Seidman^**, Jean-Claude Lavoie^** and Emile Levy^*2

Departments of ^* Nutrition, Biochemistry and ^** Pediatrics, University of Montreal and Centre de Recherche, Hôpital Sainte-Justine, Montréal, QC, Canada

²To whom correspondence should be addressed. E-mail: levye{at}justine.umontreal.ca.

We showed recently that iron + ascorbate can impair the assembly of intestinal lipoproteins. However, we could not determine whether these changes were caused by iron + ascorbate–mediated lipid peroxidation per se. We therefore conducted studies to evaluate how antioxidants antagonize the iron + ascorbate–induced derangements. To this end, Caco-2 cells, a reliable experimental intestinal model, were incubated with iron + ascorbate (0.2 mmol/L each) alone or with different concentrations of catalase, mannitol, tocopherol or BHT. Exposing Caco-2 cells to iron + ascorbate increased malondialdehyde levels fourfold (P < 0.0001); this effect was decreased markedly (P < 0.02) in the presence of BHT. Furthermore, BHT normalized the abnormal intracellular events involved in fat absorption, i.e., lipid esterification, cholesterol synthesis and apolipoprotein production. On the other hand, it did not fully restore the secretion of lipids and lipoproteins. Thus, our current data imply that iron + ascorbate–catalyzed lipid peroxidation is partially responsible for the disturbances observed in intestinal lipid transport.

KEY WORDS: • BHT • malondialdehyde • lipoproteins • apolipoproteins • Caco-2 cells

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