Administration Of Palmitate Research Articles

Comparative evaluation of macrophage stimulation and depression on tumor growth and macrophage content and function in mice

In a syngeneic murine adenocarcinoma model, the administration of glucan, an RE stimulant, inhibited tumor growth and increased tumor macrophage populations. Conversely, the administration of methyl palmitate, an RE depressant, potentiated tumor growth and decreased the number of tumor macrophages. Glucan and methyl palmitate also produced diverse alterations in serum lysozyme levels that reflected their contrasting influences on RE functional status, thus supporting the role of serum lysozyme as an index of macrophage function. The diverse results produced by macrophage stimulation or depression in regard to tumor growth, tumor macrophage population, and serum lysozyme concentration indicate that a relationship may exist between macrophage functional activity and host resistance to neoplasia.

Early bronchiolar damage following paraquat poisoning in mice.

Paraquat causes focal intracellular oedema of the terminal bronchiolar epithelial cells and focal subpleural atelectasis with thickening of the interalveolar septa 1 hr after the administration of an LD50. These changes are progressive, and lead to panacinar atelectasis with necrosis plus sloughing of epithelial cells in many terminal bronchioles. Radioactive phosphatidyl choline (PC) is recoverable by lavage within 90 s of the administration of tritiated palmitate, which supports previous suggestions that one source of pulmonary surfactant is rapid secretion by the terminal bronchiole. Paraquat causes a reduction in the relative amounts of radioactive PC that are recoverable from the airways within 90 s of giving tritiated palmitate. A deficiency of pulmonary surfactant of bronchiolar origin is implicated, at least in part, in the pathogenesis of the acute phase of the paraquat lesion in mice.

Substrate-induced membrane potential changes in the perfused rat liver

In the hemoglobin-free perfused liver, administration of pyruvate, lactate fructose, alanine and palmitate elicited a sustained hyperpolarization of the cell membrane. In contrast, glucose, galactose, lysine, acetate or α-aminoisobutyric acid had no effect on the membrane potential. The pattern of the substrate induced hyperpolarization was different from glucagon- or cyclic AMP-induced hyperpolarization in the onset and duration of the response and ouabain sensitivity. The effect of cyclic AMP (5 · 10 -4 M) on membrane potential was additive to the effect of the hyperpolarizing substrates and seems to involve a mechanism different from the substrate-induced potential changes.

Mechanism of ethyl palmitate and cobra venom factor enhancement of heterologous erythrocyte survival.

SummaryIn this study the blood survival and organ localization in rats of intravenously injected 51Cr-labeled human erythrocytes was determined in controls and following pretreatment with ethyl palmitate, a cobra venom factor, or both. Organ distribution of labeled cells was consistent with a reticuloendothelial blockade effect for the ethyl palmitate and inhibition of hemolysis for the cobra venom factor. Erythrocyte survival was enhanced only moderately following the injection of either of these substances alone. The combined administration of ethyl palmitate and the cobra venom factor, however, resulted in marked prolongation of human erythrocyte survival consistent with a synergistic effect. This suggests that in the untreated animal, both complement-dependent hemolysis and reticuloendothelial phagocytosis compete for the removal of circulating heterologous erythrocytes. Both must be blocked simultaneously for maximum heterologous erythrocyte survival.

Effect of reticulo-endothelial blockade and stimulation on hepatic mitochondrial and microsomal lipids and atherosclerosis in cholesterol-fed cockerels

Administration of methyl palmitate or India ink (RE blocking) or histamine phosphate or glycerol trioleate (RE stimulating) to cholesterol-fed cockerels did not significantly alter serum cholesterol and phospholipids. The incidence of atheroma in coronary arteries as determined microscopically was greater in histamine phosphateor glycerol trioleate-treated birds. Administration of India ink or methyl palmitate had no effect. Increase in the cholesterol levels of liver mitochondria) and microsomal fractions was observed in all the groups. The increase in microsomal cholesterol appeared to be directly correlated with the atheroma index.

An electron microscopic and functional study of very low density lipoproteins in intestinal lymph

Previous studies with fasting rats showed that the intestine produces endogenous very low density lipoproteins (VLDL) which resemble those in the plasma. Intestinal VLDL also were found to be important in lipid transport during absorption of saturated but not of unsaturated fat. These findings depended upon separations of a chylomicron-rich fraction (S(f) > 400) from VLDL (S(f) 20-400) by preparative ultracentrifugation methods based on particle flotation rates. The present studies correlate this method with electron microscopic measurement of lipoprotein particle size. Almost all intestinal lymph lipoprotein particles from fasting rats were less than 750 A in diameter, and could not be distinguished morphologically from plasma VLDL. Cholestyramine administration or bile diversion led to decreased lymph lipid output, correlating with marked reduction in VLDL. This supports the concept that lymph VLDL contain endogenous lipid which is reabsorbed from the intestinal lumen. During exogenous fatty acid absorption, lymph lipoprotein particle sizes were significantly smaller after administration of palmitate than after administration of linoleate, a finding consistent with ultracentrifugal evidence of the importance of VLDL in lipid transport during palmitate absorption. These studies fully confirm and extend earlier observations. Together, they show that the intestine is a source of endogenous VLDL in the fasting animal. In addition, significant quantities of exogenous lipid are transported in VLDL during palmitate absorption, whereas with linoleate absorption nearly all lipid is in chylomicrons. These findings indicate that the small intestine plays a role in lipoprotein metabolism which extends beyond the absorption of dietary fat.

The effect of chronic carbon tetrachlortde inhalation on the secretion of lipid by rat liver

The effect on hepatic metabolism of chronic daily 8-hr exposures of rats to 68 or 680 ppm CCl 4 vapor was studied. After 6 days of exposure there is an elevation of serum glutamic oxaloacetic transaminase and hepatic triglyceride concentration and a decrease in hepatic glycogen levels. Intravenous administration of palmitate- 14C at the end of the fifth daily exposure period to 68 ppm CCl 4 revealed a decrease in the rate of release of labeled lipid from the liver when compared to that in control animals. This was reflected in a decrease in the amount of labeled triglycerides in the serum of the intoxicated animals. After exposure to 680 ppm for 5 daily 8-hr periods, leucine-1- 14C and palmitate-9, 10- 3H were injected i.v. and the serum lipoprotein fraction was isolated. A significant decrease in the radioactivity of both lipid and protein moieties in the low density lipoproteins was noted. It was concluded that, as is the case in acute CCl 4 intoxication, chronic inhalation of CCl 4 leads to an accumulation of hepatic triglycerides and an inhibition of secretion of low density lipoproteins.

The Effect of Glucose Availability and Utilization on Chylomicron Metabolism in the Rat

AbstractFollowing i.v. administration of H3 palmitate labelled chylomicrons a greater amount of radioactivity was recovered from adipose tissue of refed than fasted rats and from insulin treated than insulin deprived diabetic rats. Adipose tissue uptake of label appeared to be potentiated by insulin in normal as well as in diabetic rats. No definite differences in the rate of clearing chylomicrons from blood was noted in insulin treated and insulin deprived diabetic rats. Although the enhanced adipose tissue uptake of triglyceride fatty acid might be related to the availability of α glycerophosphate for esterification it is equally possible that adipose tissue lipoprotein lipase content may be a regulating factor. Heparin, as opposed to saline administration prior to chyle injection, produced marked acceleration in the rate of removal of chyle from the blood of treated and untreated diabetic animals. The accelerated removal was related to accelerated uptake of activity by the liver and could be attributed in part to intravascular lipolysis of chyle triglyceride. The effect of heparin on the degree and the nature of hepatic uptake was no different in treated and untreated diabetic animals.

DEPRESSION OF PHAGOCYTIC ACTIVITY AND IMMUNE RESPONSE BY METHYL PALMITATE.

Intravenous administration of methyl palmitate produced a marked depression of the phagocytic activity of the RES. Histological evidence indicates that the RE-depressant effect exerted by methyl palmitate is not due to destruction of RE cellular elements but rather to an interference with the phagocytic activity of Kupffer cells. The functional activity of parenchymal cells was unaltered in RE hypofunctional mice. A depressed functional state of the RES, existing at the time of antigenic challenge with sheep erythrocytes, was associated with a profound inhibition of antibody formation during the primary and secondary immune response. This reduced antibody formation was not associated with alterations in the total circulating leukocyte level nor in the percentage of lymphocytes in peripheral blood. The employment of methyl palmitate to produce phagocytic and immunological paralysis is proposed.