GANGLIOSIDE COMPOSITION OF CHEMICALLY-INDUCED RAT NEURAL TUMORS AND CHARACTERIZATION OF HEMATOSIDE FROM NEURINOMAS

Abstract– Experimental rat neural tumors in offspring were induced transplacentally by a single injection of a chemical carcinogen, ethylnitrosourea, 20mg/kg body wt, in the tail vein of the mother. The ganglioside content and pattern in these tumors and the normal tissues from which the tumors originated are described. The ganglioside content in tumors was reduced, on wet tissue weight basis, compared to normal control. However, there was no significant difference of ganglioside content on dry weight or protein basis. Altered ganglioside composition was found in most of the neural tumors. In central nervous system tumors, there was some increase in GM3 and GT1b′ (nomenclature according to Svennerholm, 1963), a marked decrease in GM1 and some decrease in GD1a, but no apparent loss in GD1b. Extreme simplification of ganglioside pattern was seen in tumors originated from peripheral nervous system. Large accumulation of GM3 with concomitant loss of all the higher gangliosides was seen. GM3 from neurinomas as well as from normal gray matter was isolated and characterized. GM3 from neurinomas separated into two bands on thin layer chromatographic plates. Both these GM3 bands had identical sphingosine and carbohydrate composition but differed in their fatty acid composition. The fast moving band had 77% of the total fatty acids as C20:0 or longer chain while the slow moving band had only 22% of the long chain fatty acids. Normal gray matter GM3 had one major band containing 82% of and only 17% of the fatty acids as C20:0 or higher. It is suggested that in the tumor cells either the specificity of the enzyme cytidine monophosphate‐N‐acetyl neuraminic acid: ceramide dihexoside sialyltransferase for C18.0 fatty acid containing glycolipid was altered or that the compartmentation of precursor pools for the simpler glycolipids present in normal tissue did not exist in transformed cells. Copyright © 1979, Wiley Blackwell. All rights reserved