Effects of dietary linseed oil and marine oil on lipid peroxidation in monkey liverin vivo andin vitro

Diets rich in linoleic acid (CO) from corn oil, or in linoleic acid and either α-linolenic acid (LO) based on linseed oil or n−3 fatty acids (MO) from menhaden oil were fed to male and female Cynomolgus monkeys for 15 wk. In the liver a 40% reduction of α-tocopherol occurred in the MO group relative to the CO and LO groups followed by increased formation of lipofuscinin vivo. A four-fold increase of α-tocopherol in the MO diet (MO+E) brought the level in the liver to that found with CO and LO. The increased peroxidation in the MO group in the liver phospholipids was associated with the replacement of 60% of the n−6 fatty acids by n−3 fatty acids from menhaden oil. Similar fatty acid profiles were found in groups fed MO and MO+E, respectively. Compared to the CO fed group, feeding α-linolenic acid only resulted in a slight incorporation of n−3 fatty acids in the liver membranes mainly due to a direct incorporation of α-linolenic acid. However, in monkeys fed menhaden oil more than 30% of the total fatty acids in the liver phospholipids were n−3 fatty acids. The various diets did not influence the activity of liver catalase (EC 1.11.1.6) nor superoxide dismutase (EC 1.15.1.1), but glutathione-peroxidase activity (EC 1.11.1.9) was higher in monkeys fed the MO diet. The catalase activity in females was 20% higher than in males. In anin vitro assay, liver microsomes from monkeys fed the MO diet or the MO diet supplemented with tocopherol produced similar amounts of thiobarbituric acid reactive substances and at a much higher rate than microsomes from the CO and LO groups. It appeared that α-tocopherol did not protect long-chain n−3 C₂₀ and C₂₂ fatty acids as well as n−6 fattya acids against peroxidation. The present data showed that monkeys were not fully able to compensate for increased peroxidative stress but a four-fold supplement of vitamin E to the diets reduced the oxidation.