抄録
We hypothesized a suppressive mechanism for dietary docosahexaenoic acid (DHA)-induced tissue lipid peroxidation in which the degradation products, especially aldehydic compounds, are conjugated with glutathione (GSH) through catalysis by glutathione S-transferases (GSTs), and then excreted into urine as mercapturic acids. Sprague-Dawley rats were fed a diet containing DHA (8.4 % of total energy) for 31 days. Lipid peroxides in the liver and kidney, liver GST and urinary excretion of mercapturic acid were measured. The lipid peroxide levels in the liver and kidney except the liver aldehydic compounds were higher, and the urinary excretion of mercapturic acid also tended to be higher in the DHA-fed rats although the activity of GST was not increased after DHA intake. We presume from our results that a proportion of the lipid peroxidation-derived aldehydic degradation products might be excreted into urine as mercapturic acid after intake of DHA, thus suppressing the accumulation of aldehydic products in tissues, particularly in the liver.
