Dietary docosahexaenoic acid-induced production of tissue lipid peroxides is not suppressed by higher intake of ascorbic acid in genetically scorbutic Osteogenic Disorder Shionogi/Shi-od/od rats.
In previous studies, we showed that docosahexaenoic acid (DHA) ingestion enhanced the susceptibility of rat liver and kidney to lipid peroxidation, but did not increase lipid peroxide formation to the level expected from the relative peroxidizability index (P-index) of the total tissue lipids. The results suggested the existence of some suppressive mechanisms against DHA-induced tissue lipid peroxide formation, as increased tissue ascorbic acid (AsA) and glutathione levels were observed. Therefore, we focused initially on the role of AsA for the suppressive mechanisms. For this purpose, we examined the influence of different levels of dietary AsA (low, moderate, high and excessive levels were 100, 300 (control), 600 and 3000 mg/kg diet respectively) on the tissue lipid peroxide and antioxidant levels in AsA-requiring Osteogenic Disorder Shionogi/Shi-od/od (ODS) rats fed DHA (6.4 % total energy) for 32 or 33 d. Diets were pair-fed to the DHA- and 100 mg AsA/kg diet-fed group. We found that the lipid peroxide concentrations of liver and kidney in the DHA-fed group receiving 100 mg AsA/kg diet were significantly higher or tended to be higher than those of the DHA-fed groups with AsA at more than the usual control level of 300 mg/kg diet. Contrary to this, the liver alpha-tocopherol concentration was significantly lower or tended to be lower in the DHA and 100 mg AsA/kg diet-fed group than those of the other DHA-fed groups. However, tissue lipid peroxide formation and alpha-tocopherol consumption were not suppressed further, even after animals received higher doses of AsA. The present results suggest that higher than normal concentrations of tissue AsA are not necessarily associated with the suppressive mechanisms against dietary DHA-induced tissue lipid peroxide formation.
Sekine
Seiji
S
Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition, Toyama, Shinjuku-ku, Tokyo 162-8636, Japan.
Kubo
Kazuhiro
K
Tadokoro
Tadahiro
T
Maekawa
Akio
A
Saito
Morio
M
D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage* / Q000032:analysis; D001851:Bone Diseases, Metabolic / Q000235:genetics / Q000378:metabolism*; D004042:Dietary Fats, Unsaturated / Q000378:metabolism*; D004281:Docosahexaenoic Acids / Q000378:metabolism*; D005978:Glutathione / Q000032:analysis; D007668:Kidney / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology*; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D008297:Male; D010012:Osteogenesis / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012614:Scurvy / Q000235:genetics / Q000378:metabolism*; D013737:Testis / Q000378:metabolism; D024502:alpha-Tocopherol / Q000032:analysis
D004042:Dietary Fats, Unsaturated; D008054:Lipid Peroxides; D004281:Docosahexaenoic Acids; D005978:Glutathione; D024502:alpha-Tocopherol; D001205:Ascorbic Acid