8-11-14-eicosatrienoic-acid and Liver-Neoplasms

Incorporation and metabolism of gamma-linolenic acid (GLA) in both rat hepatocytes and Hep G2 cells were compared to those of oleic (OA), linoleic (LA), alpha-linolenic (LLA), and dihomo-gamma-linolenic (DGLA) acids. The incorporation of GLA into both types of cells was higher than LLA and DGLA, but lower than OA and LA. It was efficiently converted into DGLA in both types of cells and increased the concentration of DGLA. LLA was converted to a small amount of C20:4 (n-3) only in Hep G2 cells. Incubation with LA, GLA, LLA, and DGLA did not increase the concentration of arachidonic acid (AA) in both types of cells. LA. GLA, LLA, and their metabolites were incorporated into phosphatidylcholine, but only GLA and its metabolite, DGLA, were also incorporated into phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol. The coexistence of GLA and LLA during their catabolism diminished the amounts of respective metabolite in Hep G2 cells. The presence of GLA inhibited completely the formation of C20:4(n-3) from LLA. The results indicate that GLA is more effective in raising the ratio of DGLA/AA. Also, polyunsaturated fatty acids of n-3 and n-6 series have competitively catabolized in both types of hepatocytes.

Topics: 8,11,14-Eicosatrienoic Acid; alpha-Linolenic Acid; Animals; Carcinoma, Hepatocellular; gamma-Linolenic Acid; Humans; Linoleic Acid; Linoleic Acids; Linolenic Acids; Liver; Liver Neoplasms; Oleic Acid; Oleic Acids; Phosphatidylcholines; Phosphatidylethanolamines; Phosphatidylinositols; Phosphatidylserines; Rats; Tumor Cells, Cultured

Recent studies on the effects of the essential fatty acid metabolic intermediate, gamma-linolenic acid, on the growth of cancer cells in culture and on induced mammary cancer tumours in rats, strongly suggest that the metabolic defect in the cancer cells studied is simply a metabolic block involving the enzyme delta-6-desaturase. The latter enzyme is responsible for the conversion of linoleic acid to gamma-linolenic acid. These observations would suggest that cancer in the cell lines studied could be a relatively simple metabolic disease.

Topics: 8,11,14-Eicosatrienoic Acid; Alprostadil; Animals; Carcinoma, Hepatocellular; Cell Line; Cells, Cultured; Esophageal Neoplasms; Fatty Acid Desaturases; gamma-Linolenic Acid; Humans; Linolenic Acids; Liver Neoplasms; Melanoma; Metabolic Diseases; Mice; Neoplasms; Prostaglandins E; Scurvy

Five cases of malignant insulinoma and 2 cases of benign insulinoma were studied lipid-chemically. Tissues were collected by surgical operation or biopsy under peritoneoscopy. The total lipid was extracted from each tissue, and one part of each total lipid was separated into phospholipid, triglyceride and other lipid fractions by a thin-layer chromatography (TLC) on silica gel. The fatty acid composition and fatty acid content of each lipid fraction were measured by a gas-liquid chromatography (GLC). The most remarkable difference between malignant and benign isulinoma tissues was a higher percentage value of eicosatrienoic acid in the phospholipid of malignant insulinoma tissues when compared with that of non-malignant insulinoma tissues; the values mentioned above distributed between 9.82 and 3.32 in 5 malignant cases, but were 2.89 and 2.57 in 2 benign cases. Those changes in the phospholipid fatty acid composition of malignant insulinoma tissues may represent one of the mechanisms of malignant growth in the malignant neoplastic tissue.

Topics: 8,11,14-Eicosatrienoic Acid; Adenoma, Islet Cell; Adult; Aged; Female; Humans; Insulin; Lipids; Liver Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Pancreas; Pancreatic Neoplasms; Phospholipids; Triglycerides

Minimal deviation hepatoma 7288 C cells were cultured in Swim's medium containing 10% serum for 48 hr. The growth medium was replaced with serum free media containing different concentrations of [1-14C] eicosa-8,11,14-trienoic acid and the cells were incubated for 24 hr. Incorporation into cell lipids, oxidation to CO2, and desaturation to arachidonic acid were studied. The oxidation of the acid was very low. It was preferentially incorporated into the polar lipids of the cell. The incorporation depended on the number of cells and fatty acid concentration. Saturation of the cells with the acid was reached when 144.7 nmoles per mg of cellular protein were incorporated. The acid was desaturated readily to arachidonic acid. The nmoles of eicosatrienoic acid converted to arachidonic acid per mg of cellular protein were hyperbolic function of the acid incorporated. Maximal desaturation, 23 nmoles per mg of cellular protein, was reached when the cells were saturated with the acid. The calculations of the desaturation capacity and of the endogenous pool of eicosatrienoic acid available for desaturation in the cell are discussed.

Topics: 8,11,14-Eicosatrienoic Acid; Arachidonic Acids; Carbon Dioxide; Carcinoma, Hepatocellular; Fatty Acids, Nonesterified; Fatty Acids, Unsaturated; Lipids; Liver Neoplasms; Lysophosphatidylcholines; Neoplasms, Experimental; Oxidation-Reduction; Phosphatidylcholines; Phosphatidylethanolamines