Tumor cell lipid composition and sensitivity to humoral immune killing. I. Modification of cellular lipid and fatty acid content by metabolic inhibitors and hormones
Schlager, S.I.; Ohanian, S.H.
Journal of Immunology 124(2): 626-634
1980
ISSN/ISBN: 0022-1767 PMID: 6243329 Document Number: 168085
Metabolic inhibitors enhance and hormones decrease the sensitivity of line 10 guinea pig hepatoma cells to antibody C killing; these effects are correlated with synthesis of specific complex cellular lipids and/or fatty acids. Analysis of the lipid content of the cells showed that these changes in lipid synthesis had an influence on the mass and composition of cellular lipids and fatty acids. Drugs that render the cells susceptible to antibody C killing (adriamycin, actinomycin D) decrease unesterified cholesterol and saturated triglyceride content of the cells and increase polyunsaturated esterified cholesterol and triglyceride content compared to controls. Cardiolipin and lecithin content of these cells is also decreased, and the free fatty acid content increased compared to untreated cells. Hormones that render the cells more resistant to antibody C killing (insulin, hydrocortisone) enhance the unesterified cholesterol and saturated triglyceride content of the cells compared to controls. The hormones also lower the cardiolipin content of the cells. The drug and hormone treatments are reversible; when the cells return to control levels of susceptibility to antibody C killing, their lipid composition also returns to control levels. Drug treatment reversibly increases, whereas hormone treatment reversibly decreases the polyunsaturated fatty acid content of the cellular phospholipids. Hormone treatment also increases the total polarity of cellular fatty acids. Drug and hormone effects on the lipid and fatty acid composition of the cell could have marked effects on certain physical properties of the cell, especially membrane fluidity, permeability or thickness. These effects on physical properties of the cells could explain the drug and hormone effects on the susceptibility of the cells to humoral immune attack.