Preferential incorporation of docosahexaenoic acid into nonphosphorus lipids and phosphatidylethanolamine protects rats from dietary DHA-stimulated lipid peroxidation.
In a previous study, we found that dietary docosahexaenoic acid (DHA)-stimulated tissue lipid peroxide formation was suppressed to a lesser extent than expected from the peroxidizability index of tissue total lipids. This suppression was presumed to be potentiated by mechanisms other than the lipid peroxide-scavenging system. In this study, we focused primarily on the incorporation of DHA into tissue nonphosphorus lipids and phospholipid species. DHA and different levels of dietary vitamin E (VE; 7.5, 54, 134 and 402 mg/kg of diet) were fed to rats for 32 d. In rats with poor VE status, liver chemiluminescence intensity and kidney and testis thiobarbituric acid (TBA) values correlated with the tissue's peroxidizability index. In rats with normal VE nutriture, liver lipid peroxide formation was suppressed to a level below that expected from the peroxidizability index, likely because DHA was present in nonphosphorus lipids and utilized preferentially for phosphatidylethanolamine synthesis. In the kidney, differences in the TBA values were associated with differences in the peroxidizability index of total lipids, even in the DHA groups fed VE at higher than normal levels. This may be because the levels of lipid peroxide scavengers were lower than those of liver and because DHA was utilized preferentially for phosphatidylcholine synthesis. In testis, the lipid peroxide levels were not as high as expected from the peroxidizability index, even in rats fed a high DHA diet containing the normal level of VE. This may be because the testis was composed of a high proportion of (n-6) polyunsaturated fatty acids (PUFA), which are low in unsaturation, and thus the proportion of DHA was low. In addition, in testis, VE and ascorbic acid, which act as antioxidants, were retained at higher levels in rats with particularly poor and normal VE nutriture than those of liver and kidney. These results suggest that antioxidant protection against dietary DHA-stimulated lipid peroxidation below the extent expected from the peroxidizability index of tissue total lipids differed from tissue to tissue. The suppression was likely due to not only the lipid peroxide scavenging system but also preferential incorporation of DHA into nonphosphorus lipids and phosphatidylethanolamine, particularly in liver.
Kubo
K
K
Division of Food Science, The National Institute of Health and Nutrition, Shinjuku-ku, Tokyo 162-8636, Japan.
Saito
M
M
Tadokoro
T
T
Maekawa
A
A
D000818:Animals; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D050356:Lipid Metabolism; D015227:Lipid Peroxidation; D008163:Luminescent Measurements; D008297:Male; D010714:Phosphatidylethanolamines / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013858:Thiobarbiturates; D014810:Vitamin E / Q000378:metabolism
D005231:Fatty Acids, Unsaturated; D010714:Phosphatidylethanolamines; D013858:Thiobarbiturates; D014810:Vitamin E; D004281:Docosahexaenoic Acids; C029684:thiobarbituric acid