The role of lipid components of the diet in the regulation of the fatty acid composition of the rat liver endoplasmic reticulum and lipid peroxidation

Abstract

The fatty acid compositions of the lipids and the lipid peroxide concentrations and rates of lipid peroxidation were determined in suspensions of liver endoplasmic reticulum isolated from rats fed on synthetic diets in which the fatty acid composition had been varied but the remaining constituents (protein, carbohydrate, vitamins and minerals) kept constant. Stock diet and synthetic diets containing no fat, 10% corn oil, herring oil, coconut oil or lard were used. The fatty acid composition of the liver endoplasmic reticulum lipid was markedly dependent on the fatty acid composition of the dietary lipid. Feeding a herring-oil diet caused incorporation of 8.7% eicosapentaenoic acid (C(20:5)) and 17% docosahexaenoic acid (C(22:6)), but only 5.1% linoleic acid (C(18:2)) and 6.4% arachidonic acid (C(20:4)), feeding a corn-oil diet caused incorporation of 25.1% C(18:2), 17.8% C(20:4) and 2.5% C(22:6) fatty acids, and feeding a lard diet caused incorporation of 10.3% C(18:2), 13.5% C(20:4) and 4.3% C(22:6) fatty acids into the liver endoplasmic-reticulum lipids. Phenobarbitone injection (100mg/kg) decreased the incorporation of C(20:4) and C(22:6) fatty acids into the liver endoplasmic reticulum of rats fed on a lard, corn-oil or herring-oil diet. Microsomal lipid peroxide concentrations and rates of peroxidation in the presence of ascorbate depended on the nature and quantity of the polyunsaturated fatty acids in the diet. The lipid peroxide content was 1.82+/-0.30nmol of malonaldehyde/mg of protein and the rate of peroxidation was 0.60+/-0.08nmol of malonaldehyde/min per mg of protein after feeding a fat-free diet, and the values were increased to 20.80nmol of malonaldehyde/mg of protein and 3.73nmol of malonaldehyde/min per mg of protein after feeding a 10% herring-oil diet in which polyunsaturated fatty acids formed 24% of the total fatty acids. Addition of alpha-tocopherol to the diets (120mg/kg of diet) caused a very large decrease in the lipid peroxide concentration and rate of lipid peroxidation in the endoplasmic reticulum, but addition of the synthetic anti-oxidant 2,6-di-t-butyl-4-methylphenol to the diet (100mg/kg of diet) was ineffective. Treatment of the animals with phenobarbitone (1mg/ml of drinking water) caused a sharp fall in the rate of lipid peroxidation. It is concluded that the polyunsaturated fatty acid composition of the diet regulates the fatty acid composition of the liver endoplasmic reticulum, and this in turn is an important factor controlling the rate and extent of lipid peroxidation in vitro and possibly in vivo.

Liver Necrosis and Lipid Peroxidation in the Rat as the Result of Paraquat and Diquat Administration

“…Selenium-deficient rats from these two diet groups were given diquat. Rats fed the corn oil diet produced one-third as much ethane as those fed the cod liver oil diet, presumably because their tissues contained less omega-3 polyunsaturated fatty acid (20,21). However, evidence of liver and kidney necrosis was unaffected by the diet.…”

High Fatty Diet Effects on Rat Liver

“…The lack of a statistically significant difference between high-fat diet and the control diet in biochemical and histopathological examination, suggest that oleic acid which has been in high fat diet content of soybean oil (13) and lard (14) would have protective effect (15). In another study, it was found that soybean oil decrease lipogenesis and liver fat density (16).…”

Induction of Multidrug Resistance-Associated Protein MRP3 in the Liver of Rats Fed with Docosahexaenoic Acid

“…Peroxidation of lipids is associated with oxygen toxicity and causes degeneration of cell membranes and other lipid-containing structures, and thus is closely associated with pathologies. 5) We have shown in previous studies that the ingestion of DHA, [6][7][8][9][10] as with the ingestion of fish oil, [11][12][13][14] enhanced the susceptibility of rat liver and kidney to lipid peroxidation and increased the requirement for vitamin E (VE). This enhanced lipid peroxidation was a function of the dietary DHA level and was thought to be attributable to the replacement of membrane fatty acids with highly unsaturated DHA.…”