Lipid composition of yoshida ascites hepatoma and of livers and blood plasma from host and normal rats

Abstract

The lipid composition of Yoshida ascites hepatoma cells was analyzed together with that of ascitic plasma and of livers and blood plasma from host and normal rats. In comparison to normal livers, host livers showed no significant differences in the content of the various lipid classes, but contained a higher percentage of palmitic acid and a lower proportion of arachidonic acid in the major phospholipid classes. In addition, tumor growth induced a marked hypertriglyceridemia in host animals; changes in the concentration of other plasma lipid classes were not statistically significant. The ascitic plasma contained small amounts of lipids mainly constituted by cholesteryl esters and phospholipids. Yoshida hepatoma cells contained less phospholipids in comparison to both host and normal liver, while the increased level of triglycerides and the decrease of free fatty acids were not statistically significant. Hepatoma cells showed appreciable amounts of ether-linked lipids associated in part to neutral lipids (as glyceryl ether diesters) and, in part, to ethanolamine and choline phosphoglycerides. The alkyl groups in GEDE as well as in ethanolamine and choline phosphoglycerides were mainly constituted by C16:0 and C18:0 followed by C18:1. The alk-1-enyl groups in ethanolamine and choline phosphoglycerides were C16:0 and C18:0 with only a minor proportion of C18:1. In comparison to both host and normal liver, Yoshida hepatoma cells showed significant changes in the fatty acid composition of neutral lipids and phospholipids. Some of the major changes consisted of an increase of monoenoic acids associated with a decrease of arachidonic and docosahexaenoic acids in phosphatidylethanolamine, phosphatidylcholine, and phosphatidylinositol.

Effect of sodium selenite on lipids and lipid‐metabolizing enzymes in N‐nitrosodiethylamine‐induced hepatoma‐bearing rats

“…The lowered phospholipid content in our study was similar to that observed by Tang et al [28]. Ruggieri et al [40] have suggested a low content of total phospholipids in Yoshida hepatoma cells with a typical, fatty acid pattern in their phospholipids. The lowered phospholipid content may be the result of greater degradation, the key event in hepatomas during liver cell injury [41].…”

“…Accelerated phospholipid degradation alters the structural and functional integrity of liver cells. Also, the damaged cells become unable to repair injured membranes by regenerating new phospholipids [40]. Gross changes in phospholipid content may have serious consequences on the effective transmission of biological signals across the membrane.…”

Acinar cell carcinoma of rat pancreas: Regulation of cholesterol esterification

“…While normal tissues showed strictly regulated cholesterol synthesis, as evidenced by a drop in cholesterogenesis when cell proliferation ceased, cholesterol synthesis appeared to be deregulated in tumour cells (Rao et al, 1984a, Siperstein, 1984. Both fast and slow growing pancreatic tumours in vivo showed loss of feedback control of cholesterol synthesis and their growth rates were found to be related at least in part to their rates of.cholesterol synthesis (Rao et al, 1983;1984a (Ruggieri & Fallani, 1979). Serum cholesterol levels decreased after partial hepatectomy but not after partial pancreatectomy.…”

Composition of ether‐linked sub‐classes of glycerophospholipids in clones with a different metastatic potential isolated from a murine fibrosarcoma line (T3 cells)

“…Alkylacyl molecules were mainly associated with CGP, while alkenylacyl molecules were mostly contained in EGP, as reported in other types of transformed cells (Snyder and Wood, 1969;Ruggieri and Fallani, 1979;Fallani et al, 1982). T3 cells and their isolates, metastatic or non-metastatic, contained very small or non-detectable amounts of alkylacyl and almost the same percentages of alkenylacyl molecules in GPE.…”