title: Dietary eicosapentaenoic acid prevents systemic immunosuppression in mice induced by UVB radiation.
abstract: Moison, R. M. W. and Beijersbergen van Henegouwen, G. M. J. Dietary Eicosapentaenoic Acid Prevents Systemic Immunosuppression in Mice Induced by UVB Radiation. Radiat. Res. 156, 36-44 (2001). Reactive oxygen species (ROS) contribute to the immunosuppression induced by UVB radiation. Omega-3 fatty acids in fish oil, e.g. eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), can modulate immunoresponsiveness, but because of their susceptibility to ROS-induced damage, they can also challenge the epidermal antioxidant defense system. The influence of dietary supplementation with different omega-3 fatty acids on systemic immunosuppression induced in mice by UVB radiation was studied using the contact hypersensitivity response to trinitrochlorobenzene. In an attempt to study the mechanisms involved, UVB-radiation-induced changes in epidermal antioxidant status were also studied. Mice received high-fat (25% w/w) diets enriched with either oleic acid (control diet), EPA, DHA, or EPA + DHA (MaxEPA). Immunosuppression induced by UVB radiation was 53% in mice fed the oleic acid diet and 69% in mice fed the DHA diet. In contrast, immunosuppression was only 4% and 24% in mice fed the EPA and MaxEPA diets, respectively. Increased lipid peroxidation and decreased vitamin E levels (P < 0.05) were found in unirradiated mice fed the MaxEPA and DHA diets. For all diets, exposure to UVB radiation increased lipid peroxidation (P < 0.05), but levels of glutathione (P < 0.05) and vitamin C (P > 0.05) decreased only in the mice given fish oil. UVB irradiation did not influence vitamin E levels. In conclusion, dietary EPA, but not DHA, protects against UVB-radiation-induced immunosuppression in mice. The degree of protection appears to be related to the amount of EPA incorporated and the ability of the epidermis to maintain an adequate antioxidant level after irradiation.
authors: Department of Medicinal Photochemistry, Leiden/Amsterdam Center for Drug Research, Leiden University, Leiden, The Netherlands. moison_r@chem.leidenuniv.nl
authors: R M
authors: RM
authors: Moison
authors: G M
authors: GM
authors: Beijersbergen Van Henegouwen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000528:radiation effects; D001205:Ascorbic Acid / Q000378:metabolism; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D004817:Epidermis / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000528:radiation effects*; D005227:Fatty Acids / Q000032:analysis; D005526:Food, Formulated / Q000032:analysis; D005978:Glutathione / Q000378:metabolism; D007108:Immune Tolerance / Q000187:drug effects* / Q000276:immunology / Q000528:radiation effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010853:Picryl Chloride / Q000276:immunology / Q000494:pharmacology; D014466:Ultraviolet Rays / Q000009:adverse effects*; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005227:Fatty Acids; D014810:Vitamin E; D015118:Eicosapentaenoic Acid; D005978:Glutathione; D001205:Ascorbic Acid; D010853:Picryl Chloride