title: Different tocopherol isoforms vary in capacity to scavenge free radicals, prevent inflammatory response, and induce apoptosis in both adult- and fetal-derived intestinal epithelial cells.
abstract: Gamma-tocopherol (γ-Toc) and δ-Toc are two vitamin E isoforms for which biological activities are not well established, yet these isoforms are present in many different sources of vegetable oils and, therefore, contribute significantly to the total dietary intake of vitamin E. Infant formula also contains relatively high amounts of γ-Toc and δ-Toc, compared with that found in human milk. The efficacy of γ-Toc and δ-Toc to modulate cellular events that include oxidative stress, inflammatory response, and apoptosis-mediated cytotoxicity, relative to α-Toc, was determined using differentiated Caco-2 and primary FHs 74 Int cells intestinal epithelial cell lines. Antioxidant capacity of Toc-isoforms followed the order of δ-Toc > γ-Toc > α-Toc against peroxyl radical-induced membrane oxidation in both Caco-2 and FHs 74 Int cells, respectively. The different Toc-isoforms suppressed inflammatory response in interferon (IFN) γ/phorbol myristate acetate (PMA)-induced Caco-2 adult-derived intestinal epithelial cells, but exacerbated both IL8 and PGE2 secretion in fetal-derived FHs 74 Int intestinal epithelial cells. Lastly, Toc exhibited an isoform-dependent apoptosis-mediated cytotoxicity, whereby δ-Toc elicited the greatest apoptosis followed by γ-Toc, whereas α-Toc was not cytotoxic. Cellular uptake of non-α-Toc isoforms were greater (P < 0.05) than that observed for α-Toc in both intestinal epithelial cell lines which in part explains the superior bioactive function observed for both γ-Toc and δ-Toc, compared with α-Toc. We conclude that the non-α-Toc isoforms of vitamin E have distinct roles that influence oxidative stress and inflammatory responses in both adult and fetal-derived intestinal epithelial cell lines.
authors: Food Nutrition and Health Program, University of British Columbia, Vancouver, BC, Canada.
authors: Ingrid
authors: I
authors: Elisia
authors: David D
authors: DD
authors: Kitts
mesh_terms: D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D018938:Caco-2 Cells; D002470:Cell Survival / Q000187:drug effects; D004847:Epithelial Cells / Q000187:drug effects / Q000502:physiology*; D016166:Free Radical Scavengers / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology*; D005609:Free Radicals / Q000737:chemistry; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007413:Intestinal Mucosa / Q000166:cytology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D024505:Tocopherols / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D016166:Free Radical Scavengers; D005609:Free Radicals; D018836:Inflammation Mediators; D024505:Tocopherols
keywords: apoptosis; inflammation; intestine; oxidative stress; tocopherol