Dietary docosahexaenoic acid-induced generation of liver lipid peroxides is not suppressed further by elevated levels of glutathione in ODS rats.
OBJECTIVE
We examined the effects of ascorbic acid (AsA) and glutathione (GSH; experiment 1) and of GSH in acetaminophen-fed rats (experiment 2) on dietary docosahexaenoic acid (DHA)-induced tissue lipid peroxidation.


METHODS
In experiment 1, AsA-requiring Osteogenic Disorder Shionogi/Shi-od/od (ODS) rats were fed soybean protein diets containing DHA (10.0% total energy) and AsA at 50 (low) or 300 (normal) mg/kg without (low) or with (normal) methionine at 2 g/kg for 32 d. In experiment 2, ODS rats were fed diets containing DHA (7.8% total energy) and acetaminophen (4 g/kg) with different levels of dietary methionine (low, moderate, high, and excessive at 0, 3, 6, and 9 g/kg, respectively) for 30 d. Tissue lipid peroxides and antioxidant levels were determined.


RESULTS
In experiment 1, liver lipid peroxide levels in the low-AsA group were lower than those in the normal-AsA group, but kidney and testis lipid peroxide levels in the low-AsA group were higher than those in the normal-AsA group. Dietary methionine tended to decrease tissue lipid peroxide levels but did not decrease vitamin E (VE) consumption. In experiment 2, a high level of methionine (6 g/kg) decreased liver lipid peroxide levels and VE consumption. However, generation of tissue lipid peroxides and VE consumption were not decreased further by a higher dose of methionine (9 g/kg).


CONCLUSIONS
Higher than normal levels of dietary methionine are not necessarily associated with decreased dietary DHA-induced generation of tissue lipid peroxides and VE consumption except that the GSH requirement is increased in a condition such as acetaminophen feeding.
Division of Food Science, Incorporated Administrative Agency, National Institute of Health and Nutrition, Tokyo, Japan.
Seiji
S
Sekine
Kazuhiro
K
Kubo
Tadahiro
T
Tadokoro
Morio
M
Saito
D000082:Acetaminophen / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000494:pharmacology; D001851:Bone Diseases, Metabolic / Q000235:genetics / Q000378:metabolism; D004042:Dietary Fats, Unsaturated / Q000378:metabolism*; D004281:Docosahexaenoic Acids / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000008:administration & dosage* / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008054:Lipid Peroxides / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism; D008297:Male; D008715:Methionine / Q000008:administration & dosage / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D011919:Rats, Inbred Strains
D004042:Dietary Fats, Unsaturated; D008054:Lipid Peroxides; D004281:Docosahexaenoic Acids; D000082:Acetaminophen; D008715:Methionine; D005978:Glutathione; D001205:Ascorbic Acid