[Various quantities of sunflower seed oil in the diet, long-term administration of hydrocortisone and liver tissue lipids in rats]. / Razlicite kolicine suncokretovog ulja u ishrani, dugotrajna primena hidrokoritzona i lipidi tkiva jetre pacova.

The influence of different quantities of vegetable oil/sunflower oil/and the long-term ingestion of hydrocortisone on the total lipid content of the liver in rats and cholesterol was studied. The rats were of Wistar strain, males, 2 months old at the beginning of the experiment. The sunflower oil comprised 5 g%/diet A/ and 20 g%/diet B/ in the diet of rats. Two groups of animals were on diet A or B and took as much water as required. Another two experimental groups were on similar diets A or B, with an additional ingestion of 0.5 mg/kg of hydrocortisone natrium-succinate over the whole period of experiment. The experiment lasted 6 months. The study showed that the major participation of the sunflower oil/20 g%/ induced the increase of the total lipid content of the liver, with significant increase of cholesterol. Long-term ingestion of glucocorticosteroids/hydrocortisone natrium-succinate/induced the significant increase of the content of total lipids and cholesterol in the liver tissue in rats, independent of ingestion of sunflower oil in diet.

Phospholipid and ganglioside composition in rat cerebral cortex and cerebral white matter after chronic diazepam treatment.

Male Wistar rats with an initial weight of 170 g were maintained on a nutritionally adequate diet, and diazepam was administered in a dose of 10 mg/kg/d. Control animals were pair-fed on adequate diet. The feeding was continued for 180 days, and the effects on cerebral cortex and white matter lipid contents were studied. A generalized increase in the lipid phosphorus and lipid-N-acetylneuraminic acid (NeuAc) level was found. The increase was statistically significant for phosphatidylethanolamine and phosphatidylserine, ganglioside GM1, GD1a and GDIb in the cerebral cortex, as well as for phosphatidylinositol and phosphatidic acid in the cerebral white matter. There were no significant differences in the content and patterns of gangliosides in the cerebral white matter after the chronic diazepam treatment.

Brain lipids in rat after chronic diazepam treatment.

Male Wistar rats with an initial weight of 170g were maintained on a nutritionally adequate diet, and diazepam was administered at a dose of 10 mg/kg/d. Control animals were pair-fed an adequate diet. The feeding was continued for 180 d, and the effects on brain lipid contents were studied. It was found that the contents of the phospholipids, phosphatidylethanolamine and phosphatidylserine, the monogalactosyl glycolipids, hydroxy and nonhydroxy fatty acyl galactocerebroside, sulfoglycolipids, and the gangliosides, GM1, GD1a, GD1b, and GT1b, were significantly reduced in the brain of diazepam-treated rats. There was a significantly increased content of phosphatidylinositol after 180 d of diazepam treatment. The results suggest that changes in brain lipid content may mediate the adaptive changes that occur upon prolonged exposure to diazepam.

Influence of high-protein diets on brain phospholipid, ganglioside and monogalactosyl glycolipid content previously altered by long-term low-protein and ethanol administration.

A previous study was undertaken to determine the influence of the combined effects of ethanol consumption and a low-protein diet on brain membrane (phospholipids and gangliosides) and myelin (monogalactosyl glycolipids) lipids. Male Wistar rats chronically consuming ethanol were fed isoenergetic diets containing 22% protein (controls) or 6% protein (protein-deprived) from 60 to 240 days of age. Protein malnutrition initiated at 60 days of age affected phosphatidylglycerol, sphingophospholipid, monosialoganglioside GM1 and cerebroside containing nervonic fatty acid by 240 days of age. Among the effects of ethanol was an increase of the relative proportion of lipid galactose in monogalactosyl glycolipids and of N-acetylneuraminic acid in the trisialoganglioside GT1b, while there was decrease of the lipid phosphorus in the investigated phospholipids and of the disialoganglioside GD1a. The low-protein diet generally interfered with ethanol effects except for monosialo GM3, GM2 and GM1 gangliosides. The present study was carried out to investigate whether the ethanol-induced effect on these brain lipids could be elevated when we switched these animals to diets with 21 or 34% protein during the following 90 days. It was found that increasing protein intake and cessation of drinking ethanol returned the investigated brain phospholipids, monogalactosyl glycolipids and gangliosides to control values.