Effects of dexamethasone on lipid metabolism in rat organs

Injecting of dexamethasone (10 mg/kg body weight) for 8 days to rats decreased the body weight and feed intake by 29 and 50%, respectively. The increase in weights of liver, heart, kidneys and testes per 100 g body weight was 55, 37, 33 and 13%, respectively. Though, in general, the triglyceride content increased in all the organs, maximum increase (9-fold) was observed in the liver. The plasma showed elevated levels of triglycerides, cholesterol and phospholipids. In hepatic mitochondrial membranes, the content of protein, phospholipids and cholesterol decreased/g tissue. The percent 14C distribution, as a part of total incorporation in nonpolar lipids, of [14C]acetate into triglycerides of liver, kidneys and testes increased significantly. The increased turnover of phospholipids in liver and heart was mainly due to increased turnover of phosphatidyl choline (PC) and phosphatidyl ethanolamine in liver and PC in heart. Turnover of phospholipids of testes was not affected.     

Effect of Feeding Defatted Millet (Sorghum vulgarie) Flour at Different Protein Levels on Phospholipids of Rat Liver

Effect of feeding defatted millet flour at 5, 10 and 14.5 percent protein levels respectively to rats for 6 weeks has been studied on their liver phospholipids. Feeding of millet at these protein levels significantly increased liver total lipids and total glycerides as compared to control rats fed casein at 10 percent level. Liver phospholipids and phosphatidyl choline were significantly increased in rats fed millet at 10 and 14.5 percent protein levels whereas phosphatidyl ethanolamine was increased in all millet protein fed groups. Incorporation of (counts/liver/100 g body weight) into liver total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine was significantly increased in M–5 and M–15% groups and it was decreased in phosphatidyl choline in rats of M–10% groups as compared to control. The effects of feeding millet on liver phospholipids are due to the quantity as well as quality of the millet protein.     

Effect of Retinol on Liver Lipid Metabolism of Rats

Effect of feeding 4.23, 16.94 and 27.53 mg of retinol daily for 10 days on the liver lipids of adult rats has been studied. Feeding of different amounts of retinol produced dose dependent toxicity symptoms in rats. Retinol feeding resulted in significant elevations of liver total lipids, total fatty acids, and glycerides, The amounts of liver esterified cholesterol were significantly raised in rats fed different amounts of retinol. Acetate-1-¹⁴C incorporation was increased in liver total cholesterol of rats fed 27.53 mg retinol and in free cholesterol of all retinol fed rats. Total ¹⁴C activity of hepatic triglycerides of retinol fed rats was the same as that of control, but their specific activity was decreased. Significant alterations were noted in phosphatidyl serine, lysophosphatidyl choline, lysophosphatidyl ethanolamine, sphingomyelin, phosphatidyl choline, phosphatidyl ethanolamine and phosphatidic acid and polyglycerophosphate fractions in liver rats fed different amounts of retinol.     

In vitro incorporation of [14CH3]methionine into liver phosphatidylcholine in rats with vitamin E deficiency

The content of phosphatidyl choline, a terminal product of phosphatidyl ethanolamine methylation as well as in intensity in vitro incorporation of [14CH3]methionine into phosphatidyl choline of rat liver with E-hypovitaminosis are found to considerably decrease as compared to the norm. In this case the total content of phospholipids is practically the same.     

Incorporation of [1-14C]Palmitic Acid into Neutral Lipids and Phospholipids of Rat Cerebral Cortex In Vitro

Abstract: Incorporation of [1-¹⁴C]palmitic acid into neutral lipids and phospholipids of rat cerebral cortex was examined in vitro in normal Krebs-Ringer bicarbonate buffer containing 3% (wthol) albumin and 0.75 mM palmitic acid. Under standard assay conditions, radioactivity in the triacylglycerol fraction increased rapidly during the first 30 min, and then decreased after 60 min, with corresponding increase in radioactivity in phosphatidyl choline, phosphatidyl ethanolamine, and a fraction of phosphatidyl inositol plus phosphatidyl serine. Diacylglycerol was shown to be an intermediate metabolite. Radioactivity increased in triacylglycerol, and decreased in phosphatidyl choline and phosphatidyl ethanolamine throughout incubation under NZ gas. In the fraction of phosphatidyl inositol plus phosphatidyl serine, radioactivity decreased after 30 min during incubation under N, gas. A possible acylation-deacylation cycle, in which triacylglycerol could be a source of free fatty acids for phospholipids, is discussed.     

Hepatic Subcellular Fractions Lipids in Rats Fed Millet (Sorghum vulgarie) at Different Protein Levels

Effect of feeding defatted millet (Sorghum vulgarie) flour at 5, 10 and 14.5% protein levels respectively for six weeks has been studied on rat liver mitochondrial, microsomal and supernatant fractions total lipids, cholesterol, triglycerides, total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine. The results have been compared with rats fed casein at 10% level for the same period. The metabolism of liver subcellular fractions lipids of millet diet and casein diet fed rats has been studied by the incorporation of acetate-1-¹⁴C and . A significant increase in mitochondrial triglycerides of rats fed millet diet at 5 and 10% protein level, in microsomes of rats fed millet diet at 5, 10 and 15% protein levels and in supernatant fractions of rats fed millet diet at 5 and 15% protein levels was observed. A significant increase in total cholesterol in mitochondria and microsomes and a significant decrease in supernatant fraction of rats fed millet diet at 10% protein level was observed. A significant increase in mitochondrial total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine in rats fed millet diet at 10% protein level and a decrease in these in rats fed millet diet at 5 per cent protein level was observed. In microsomes total phospholipids were increased in rats millet diet at 10% protein level and phosphatidyl choline was increased in rats fed millet diet at 15% protein level. Total phospholipids, phosphatidyl choline and phosphatidyl ethanolamine were significantly reduced in the supernatant fraction of rats fed millet at 10% protein level.

Incorporation of acetate-1-¹⁴C into nonsaponifiable fraction of mitochondria, microsomes and supernatant fractions of rats fed millet diet at 5 and 15 % protein levels was significantly greater, and in saponifiable fractions of the above subcellular fractions was greater in rats fed millet diet at 5 per cent protein level. The specific activity (counts/min/mg) of free cholesterol in mitochondria, microsomes and supernatant fractions of millet diet fed rats was significantly greater, whereas the specific activity of triglycerides was not significantly different from the controls. The acetate-1-¹⁴C specific activity of phosphatidyl choline and phosphatidyl ethanolamine was significantly greater in all the above subcellular fractions of millet diet fed rats (except of phosphatidyl choline in rats fed millet diet at 5 % protein level). The specific activities of phosphatidyl choline were significantly greater in mitochondria of rats fed millet diet at 5 % protein level and of phosphatidyl choline and phosphatidyl ethanolamine in microsomes and supernatant fractions of rats fed millet diet at 5 and 15% protein levels. The specific activities of phosphatidyl choline were significantly decreased in mitochondria and microsomes of rats fed millet diet at 10% protein level. The total acetate-1-¹⁴C activities (counts/min/g equivalent wet liver) of free and esterified cholesterol triglycerides, phosphatidyl choline and phosphatidyl ethanolamine showed that their synthesis from acetate-1-¹⁴C was either enhanced in millet diet fed rats or was comparable to the controls. The total activity of (counts/min/g equivalent wet liver) into phosphatidyl choline and phosphatidyl ethanolamine showed that their synthesis was decreased in microsomes of rats fed millet diet at 10% protein level, increased in rats fed millet diet at 5 and 15% protein levels.     

In vivo studies on pathways for the biosynthesis of lecithin in the rat

The in vivo biosynthesis of lecithin in rats has been studied with the precursors choline-1,2-(14)C, ethanolamine-1,2-(14)C and methionine-CH(3)-(14)C or -CH(3)-(3)H. Lecithin synthesis from choline is rapid in all organs. No sex difference was observed in this pathway. The biosynthesis of lecithin by methylation of phosphatidyl ethanolamine is of quantitative significance in the liver, but not in extrahepatic tissues. More lecithin is synthesized by this pathway in female rats. In liver the lecithin synthesized via both pathways enters a common pool which is in rapid equilibrium with lecithin of blood plasma. A sex difference in the utilization of radioactive ethanolamine for the formation of phosphatidyl ethanolamine was observed (greater utilization in the female). Incorporation of ethanolamine into phospholipids of extrahepatic tissues was slow in both sexes. With labeled methionine as precursor the liver cytidine diphosphate (CDP) choline had a specific activity identical with that of liver lecithin after 20 min, while the specific activity of phosphoryl choline remained low. With labeled choline as precursor the phosphoryl choline reached a specific activity 50 times that of lecithin after 20 min, while the specific activity of CDP choline was only four times that of lecithin. These findings indicate that the reaction: CDP choline + diglyceride right harpoon over left harpoon phosphatidyl choline + CMP is freely reversible in vivo.     

Inhibition of chilling-induced photooxidative damage to leaves of Cucumis sativus L. by treatment with amino alcohols

The effect of pretreatment of cucumber (Cucumis sativus L.) roots with choline chloride or ethanolamine on leaf phospholipid composition and light-induced leaf damage during chilling was studied. Photooxidative chlorophyll degradation was similarly inhibited by both amino alcohols. The decrease of the chlorophyll a/chlorophyll b ratio and the increase of polyunsaturated-fatty-acid degradation during chilling in the light were equally inhibited by pretreatment with choline chloride or ethanolamine. Treatment with choline chloride and ethanolamine caused, respectively, 43% and 26% increases in the total phospholipid contents of the leaves. After treatment with choline chloride, the phosphatidylcholine content was higher than the content of phosphatidylethanolamine; the reverse was true after treatment with ethanolamine. The chlorophyll concentration increased less than the phospholipid concentration, resulting in a decreased chlorophyll/phospholipid ratio of treated leaves. During chilling in the light, degradation of phosphatidylcholine, ethanolamine and phosphatidyl glycerol occurred. Phosphatidyl glycerol was less sensitive than phosphatidylcholine and ethanolamine. The degradation was equally inhibited by pretreatment with either amino alcohol. Possible connections between the phospholipid content of leaf membranes and the inhibition of chilling-induced photooxidative leaf damage are discussed.Abbreviations CC choline chloride - Chl chlorophyll - EA ethanolamine - PC phosphatidyl choline - PE phosphatidyl ethanolamine - PG phosphatidyl glycerol     

LECITHIN SYNTHESIS, INTRACELLULAR TRANSPORT, AND SECRETION IN RAT LIVER : IV. A Radioautographic and Biochemical Study of Choline-Deficient Rats Injected with Choline-3H

Injection of choline-³H into choline-deficient rats resulted in an enhanced incorporation of the label into liver lecithin, as compared to the incorporation of label into liver lecithin of normal rats. The results obtained with the use of different lecithin precursors indicate that in the intact liver cell, both in vivo and in vitro, exchange of choline with phosphatidyl-choline is not significant. The synthesis and secretion of lecithins by the choline-deficient liver compare favorably with the liver of choline-supplemented rats, when both are presented with labeled choline or lysolecithin as lecithin precursors. Radioautography of the choline-deficient liver shows that 5 min after injection of choline-³H the newly synthesized lecithin is found in the endoplasmic reticulum (62%), mitochondria (13%), and at the "cell boundary" (20%). The ratio of the specific activity of microsomal and mitochondrial lecithin, labeled with choline, glycerol, or linoleate, was 1.53 at 5 min after injection, but the ratio of the specific activity of phosphatidyl ethanolamine (PE), labeled with ethanolamine, was 5.3. These results indicate that lecithin and PE are synthesized mainly in the endoplasmic reticulum, and are transferred into mitochondria at different rates. The site of a precursor pool of bile lecithin was studied in the intact rat and in the perfused liver. Following labeling with choline-³H, microsomal lecithin isolated from perfused liver had a specific activity lower than that of bile lecithin, but the specific activity of microsomal linoleyl lecithin was comparable to that of bile lecithin between 30 and 90 min of perfusion. It is proposed that the site of the bile lecithin pool is located in the endoplasmic reticulum and that the pool consists mostly of linoleyl lecithin.     

Phospholipids of rat tissues after feeding pure phosphatidyl ethanolamine and lecithin

Pure phosphatidyl ethanolamine and lecithin from egg yolks were fed to rats in saline or in olive oil and the changes in individual phospholipids in the intestinal wall, liver, and plasma of the animals were studied. Ingestion of olive oil alone produced increased levels of all phospholipid fractions in each of the three tissues. Feeding phosphatidyl ethanolamine in saline resulted in slightly increased plasma phospholipids, but levels of liver total phospholipids were greatly reduced; when phosphatidyl ethanolamine was fed with olive oil, liver phospholipids were again reduced but this reduction was confined to the phosphatidyl ethanolamine and phosphatidic acid fractions. Feeding lecithin alone did not produce significant changes in levels of plasma or tissue phospholipids. The results suggest that liver phospholipid synthesis is depressed by feeding phosphatidyl ethanolamine; in the presence of olive oil, hepatic synthesis of phosphatidyl ethanolamine seems to be more selectively inhibited.     

Phospholipid and ether linked phospholipid content alter with cellular resistance to vinblastine

The phospholipid and ether linked phospholipid content of leukaemic lymphocytes alters when the cells become resistant to low levels of the anti-cancer drug, vinblastine. Sphingomyelin and cardiolipin increase, and phosphatidyl ethanolamine and serine decrease in resistant cells. In addition, increases in 1-alkyl-2-acyl phosphatidyl choline and 1-alkenyl-2-acyl-phosphatidyl ethanolamine are concomitant with decreased 1,2-diacyl phosphatidyl choline and ethanolamine. Changes to the ultrastructure of the inner half of the plasma membrane bilayer, as a consequence of drug resistance, are illustrated by freeze-fracture electron microscopy.     

Characterization of gastric mucosal membranes: lipid composition of purified gastric microsomes from pig, rabbit, and frog

The lipid compositions of the gradient-purified gastric microsomal membranes from the fundic mucosa of pig, rabbit, and frog were determined. The total lipid content varied widely. Compared to the rabbit (21.6 ± 0.6 mg/100 mg protein), the pig had about twice as much and the frog about three times as much lipid. The levels of cholesterol were higher in both mammalian species (about 32% of the lipid) compared to frog (23%). Phospholipids accounted for about 45, 54, and 52% of the total microsomal lipids from pig, rabbit, and frog and the molar ratios of cholesterol to phospholipid in the three species were 1.95, 1.6, and 1.17, respectively. Phosphatidyl choline and phosphatidyl ethanolamine together constituted about 75% of the total phospholipids in pig and frog and 93% in rabbit gastric microsomes. Sphingomyelin comprised 19.3, 3.2, and 1.5% in pig, rabbit, and frog, respectively. Phosphatidyl inositol constituted 5, 2.7, and 23.6% in pig, rabbit, and frog, respectively. The ratios of phosphatidyl ethanolamine to phosphatidyl choline were 1.17, 1.1, and 0.85 in pig, rabbit, and frog, respectively. The saturated fatty acids 16:0 and 18:0 and the unsaturated fatty acid 18:1 and 18:2 were the predominant fatty acids in all phospholipids. The ratios of saturated to unsaturated fatty acids were between 0.8 and 0.9 in phosphatidyl choline and 0.27 and 0.5 in phosphatidyl ethanolamine from all three species. The contributions by saturated fatty acids were much more in phosphatidyl inositol and sphingomyelin than in phosphatidyl choline and phosphatidyl ethanolamine from all species. Position 1 of phosphatidyl choline had 63% saturated and 37% unsaturated fatty acids; while the reverse was true for position 2. Phosphatidyl ethanolamine, however, had 85% saturated fatty acids in position 1 compared to only 25% in position 2. Arachidonic acid (20:4) was present in significant amounts in all species located exclusively at position 2 of both phosphatidyl choline and phosphatidyl ethanolamine.     

The molecular organization of nerve membranes

Summary The lipid content and composition from an axolemma-rich preparation isolated from squid retinal axons was analyzed.The lipids, which accounted for 45.5% of the dry weight of this membrane, were composed of 22% cholesterol, 66.7% phospholipids and 5.2% free fatty acids. The negatively charged species phosphatidyl ethanolamine (37%), phosphatidyl serine (10%) and lysophosphatidyl ethanolamine (4%) made up 51% of the phospholipids. The amphoteric phosphatidyl choline and sphingomyelin accounted for 39% and 4%, respectively.The relative distribution of fatty acids in each of the isolated phospholipids was studied. The most remarkable feature of these phospholipids was the large proportion of long-chain polyunsaturated fatty acids. The 226 acyl chain accounted for 37% in phosphatidyl ethanolamine, 21.7% in phosphatidyl choline, 17.5% on phosphatidyl serine and 20.3% in sphingomyelin (all expressed as area %).The molar fraction of unsaturated fatty acids reached 65% in phosphatidyl ethanolamine and 42.0 and 44.8% in phosphatidyl choline and phosphatidyl serine, respectively. The double bond index in these species varied between 1.0 and 2.6.The lipid composition of the axolemma-rich preparation isolated from squid retinal axons appears to be similar to other excitable plasma membranes in two important features: (a) a low cholesterol/phospholipid molar ratio of 0.61; and (b) the polyunsaturated nature of the fatty acid of their phospholipids.This particular chemical composition may contribute a great deal to the molecular unstability of excitable membranes.The preceding papers of this series were published inArchives of Biochemistry and Biophysics.     

Cytolysis of nucleated cells by complement: inhibition of membrane-transmethylation enhances cell death by C5b-9

Inhibition of transmethylation, i.e., enzymatic transfer of methyl groups to phosphatidyl ethanolamine resulting in generation and translocation of phosphatidyl choline, enhances the killing of nucleated cells by complement. Furthermore, under complement attack, transmethylation measured as incorporation of [3H]methyl groups into phosphatidyl choline is enhanced, suggesting that transmethylation functions as a membrane defense mechanism either by increasing the phosphatidyl choline synthesis or by transducing a signal that might trigger another membrane repair process.     

Local and metastatic tumor growth and membrane properties of LM fibroblasts in athymic (nude) mice

LM fibroblasts grown in a chemically-defined, serum-free medium readily incorporated choline or one of three analogues of choline, namely N,N-dimethylethanolamine, N-monomethylethanolamine, or ethanolamine into membrane phospholipids. The effect of these phospholipid manipulations in vitro on tumor growth and metastasis was examined in nude mice. Serum and choline-fed cells most frequently metastasized (74% and 68%, respectively), while frequency of lung metastasis was 46%, 42% and 17% in mice injected with cells fed with dimethylethanolamine, monomethylethanolamine, and ethanolamine, respectively. Metastases from cells cultured with serum, choline or dimethylethanolamine, but not from monomethylethanolamine or ethanolamine, were extensive and highly invasive. The specific activity of the (Na+ + K+)-ATPase but not of 5'-nucleotidase was significantly decreased in local tumor plasma membranes from choline analogue-fed cells as compared to tumor plasma membranes from choline-fed cells. When compared to the choline-fed tumor cells, the specific activities of three mitochondrial enzymes, namely NADH dependent, rotenone insensitive NADH-dependent, and rotenone sensitive NADH-dependent cytochrome-c reductase, were significantly increased in the choline analogue-supplemented cells. The arachidonic acid content of phosphatidylcholine in plasma membranes, microsomes, and mitochondria was significantly decreased in tumor membranes from choline analogue-fed cells as compared to tumor membranes from choline-fed cells. As compared to local tumor plasma membranes, the lung metastasis plasma membranes had elevated (Na+ + K+)-ATPase specific activity, phospholipid oleic and arachidonic acid content, and fluidity. In contrast, the 5'-nucleotidase specific activity, the content of cholesterol, phospholipid, and phosphatidylethanolamine were decreased in lung metastasis plasma membranes. In summary, membrane alterations of LM tumor cells in vitro (1) were not completely reversed in vivo, and (2) affected metastatic ability.     

Effect of Temperature and BASF 13 338 on the Lipid Composition and Respiration of Wheat Roots

The fatty acid composition of wheat seedling roots changed in response to temperature. As temperature declined, the level of linolenic acid increased and the level of linoleic acid decreased. The distribution of phospholipid classes was not influenced by temperature. Phosphatidyl choline and phosphatidyl ethanolamine were the predominant phospholipids isolated and comprised 85% of the total lipid phosphorus. Smaller quantities of phosphatidyl glycerol, phosphatidyl inositol, phosphatidic acid, and phosphatidyl serine were isolated. The fatty acid composition of phosphatidyl choline and phosphatidyl ethanolamine were the same and temperature affected the fatty acid composition of both phospholipids in the same manner.Growth in the presence of the substituted pyridazinone, BASF 13 338 (4-chloro-5-dimethylamino-2-phenyl-3(2H)pyridazinone), reduced the level of linolenic acid and increased the level of linoleic acid in the phosphatidyl choline, phosphatidyl ethanolamine, and total polar lipid fractions. BASF 13 338 did not affect the levels of palmitate, stearate, and oleate or the distribution of phospholipid classes.Respiration rates of wheat root tips were measured over a range of temperatures. The respiration rate declined as the temperature decreased. Neither the temperature at which the tissue was grown nor BASF 13 338 treatment influenced the ability of root tips to respire at any temperature from 4 to 30 C. The results indicated that the relative proportion of linolenic acid to linoleic acid did not influence the plants ability to grow and respire over the range of temperatures tested.     

Isolation and characterization of plamsa membrane from monolayer cultures of epitherlial type II lung cells.

Pneumocyte type II produces a phospholipid, dipalmitoyl lecithin, which is stored in and secreted from the cell's inclusion bodies and is indispensable for alveolar stability. Cloned rat lung type II cells were harvested at monolayer confluence and homogenized in swelling buffer. After sequential differential centrifugations, the crude membrane fraction was subjected to discontinuous sucrose density gradient centrifugation at 65,000 × g. Quality of the relevant fractions was monitored by enzyme activities and phase contrast and electron microscopy of two major bands at densities 1.16 and 1.18, respectively. The less dense band contained only small quantities of organelles, little cytochrome c oxidase, and some glucose 6-phosphatase, but had a significant (Na⁺, K⁺)-ATPase activity; this and ultrastructural evidence certified the product as a suitable plasma membrane preparation. Upon sodium dodecyl sulfate-poly acrylamide gel electrophoresis, the protein pattern consisted of 11 major protein bands between 13,000 and 68,000 M_r ranges, and several minor ones. The lipid pattern was studied by two-dimensional thin layer chromatograpy, followed by various group reactions (e.g., amine, unsaturation, phosphorus, sugars). In the two major phospholipids, phosphatidyl choline and phosphatidyl ethanolamine, palmitic acid was the least abundant of four major fatty acids, accounting for 14.20% in phosphatidyl choline and 5.70% in phosphatidyl ethanolamine, whereas the most abundant were stearic and palmitoleic with about 28% each in phosphatidyl choline, and palmitoleic (29.90%) and oleic (23.05%) in the ethanolamine phosphatide. Apparently, the palmitic acid containing phosphatidyl choline must be in the lamellar inclusion bodies of type II cells and not in their plasma membranes.     

Isolation and characterization of a Chinese hamster ovary cell line requiring ethanolamine or phosphatidylserine for growth and exhibiting defective phosphatidylserine synthase activity

A mutant cell line (designated M.9.1.1) requiring ethanolamine for growth was derived from Chinese hamster ovary (CHO-K1) cells using 5-bromodeoxyuridine enrichment. The ethanolamine requirement was readily replaced by 20 microM phosphatidylserine and 10 microM lysophosphatidylethanolamine. When M.9.1.1 cells were supplemented with phosphatidyl[3H]serine it was rapidly taken up, and subsequently decarboxylated to form phosphatidyl[3H]ethanolamine. The incorporation of [3H]serine into phosphatidylserine in the mutant cells was 57% of that in the parental cells. Phosphatidylethanolamine synthesis from [3H]serine in the mutant cells was 35% of that in parental cells. When M.9.1.1 cells were deprived of ethanolamine for 48 h the level of phosphatidylserine decreased 34% and the level of phosphatidylethanolamine decreased 26% compared to parental cells. At the same time the rate of turnover of phosphatidylserine was reduced to half that found in parental cells. Examination of the enzymes of phosphatidylserine metabolism indicated defective phosphatidylserine synthase activity in the mutant. When exogenous phosphatidylcholine was used as the phospholipid substrate for the reaction the apparent kinetic constants were Vmax (mutant) = 5.7 pmol/min/mg protein and Vmax (parental) = 17.5 pmol/min/mg protein. Measurement of the back reaction (ATP-independent incorporation of choline into phospholipid) gave no detectable activity in the mutant cells. The data indicate that the phosphatidylcholine-dependent synthesis of phosphatidylserine is the primary lesion in M.9.1.1.     

Myocardial lipid metabolism in cardiac hyper- and hypo-function. Studies on triiodothyronine-treated and transplanted rat hearts.

Lipid composition of the myocardium and in vitro lipid metabolism were studied in hearts from young rats after 30 days of treatment with triiodothyronine (100 microgram/kg per day) and in heterotopically isotransplanted hearts of inbred adult rats 6 days after surgery. The former served as an experimental model of cardiac hyperfunction, while the latter, empty beating hearts, served as a model of cardiac hypofunction. In hearts from hyperthyroid animals the concentration of phosphatidylcholine, phosphatidylethanolamine, cardiolipin, and the incorporation of 14C-labelled palmitic and erucic acid into these phospholipids were increased significantly as compared with controls. In contrast, the triglyceride concentration and the incorporation of palmitate into triglyceride was significantly decreased. In transplanted hearts, the phospholipid concentration and the incorporation of 14C-labelled fatty acids into phospholipids were significantly decreased as compared with the hearts of the inbred host rats of the same age. The results indicate that the mechanical performance of the heart affects the phospholipid composition, which may be a reflection of increased or decreased proliferation of subcellular membranes in sustained cardiac hyper- or hypo-function.     

Changes in phospholipids and free fatty acids in the brains of mice preconditioned by hypoxia.

Changes in the composition and contents of phospholipids and free fatty acids were observed and compared in three groups: (A) unpreconditoned normal controls, (B) exposure to 1 run of hypoxia and (C) exposure to 4 runs of hypoxia. In group B, the content of phosphatidyl ethanolamine (PE), phosphatidyl serine (PS) and free fatty acids (FFAs) increased significantly and the content of phosphatidyl choline (PC) and sphingomyelin (SM) decreased significantly. While in group C the content of PE, PS, PC and FFAs changed significantly when compared with that of group B, all phospholipid (except SM) and FFA contents tended to decrease to the level of group A. No new FFA was seen in the brain homogenates in any of the three groups. These results suggest that the changes in the content of mouse brain phospholipids and FFAs may be adaptive and involved in the animals' tolerance to hypoxia.