Preparation of hydroperoxy and hydroxy derivatives of rat liver phosphatidylcholine and phosphatidylethanolamine

A convenient method for the preparation of hydroperoxy and hydroxy derivatives of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) is described. PC and PE obtained from rat liver were oxidized with singlet oxygen by using methylene blue as the photosensitizer, and their hydroperoxides were isolated with the aid of reverse phase liquid chromatography. The hydroxy derivatives were obtained by reducing the hydroperoxides with sodium borohydride. The results of gas chromatography mass spectrometry revealed that hydroxy fatty acid components of the hydroxy derivatives were derived from isomeric hydroperoxides of oleic acid, linoleic acid, arachidonic acid and docosahexanoic acid. Normal phase high performance liquid chromatography did not separate the hydroperoxy and hydroxy derivatives from the respective unoxidized phospholipids, although unoxidized PC and PE were separated from each other. However, the hydroperoxy and hydroxy derivatives could be distinguished from unoxidized phospholipid species on reversed phase thin layer chromatography.     

Effects of dietary protein and cholesterol on phosphatidylcholine and phosphatidylethanolamine molecular species in mouse liver

The present study examined the effects of two atherogenic factors, animal protein and cholesterol, on the distribution of fatty acids and the molecular species of major liver phospholipids in mice. Weanling mice were fed a semisynthetic diet supplemented with either casein or soy protein (20%, w/w) in the presence or absence of 0.5% cholesterol for 4 wk. Results from mouse liver showed that animal protein and, more so, dietary cholesterol modified the fatty acid profiles of the phospholipids. Animal protein had no significant effect on the concentration of lipids, but it altered the relative distribution and fatty acid profiles of the phospholipids, phosphatidylcholine and phosphatidylethanolamine. Dietary cholesterol, on the other hand, significantly increased the concentration of liver lipids, but it did not alter the relative distribution of phosphatidylcholine and phosphatidylethanolamine. In cholesterol-fed mice, the proportions of molecular species containing 18∶2n−6 were increased, whereas those containing 20∶4n−6 were decreased, indicating that dietary cholesterol suppressed linoleic acid metabolism. Since cholesterol feeding selectively decreased the ratio of 18∶0/20∶4n−6 in phosphatidylcholine, whereas it increased the 18∶0/18∶2n−6 ratio in phosphatidylethanolamine, this finding suggests that dietary cholesterol may affect the incorporation of fatty acids but not the rate of synthesis of phosphatidylcholine and phosphatidylethanolamine.     

Lipid composition of liver mitochondria and microsomes in hyperthyroid rats

Triiodothyronine-induced alteration of the lipid pattern in rat-liver mitochondria and microsomes has been investigated. In mitochondria, a 25% total cholesterol decrease and a 14% phospholipid increase have been detected. In these hyperthyroid rat liver organelles, a strong decrease in the total cholesterol/phospholipid molar ratio occurs. On the contrary, in microsomes from the same animals, a decrease of about 23% has been measured for both total cholesterol and phospholipids; hence, in this fraction, the total cholesterol/phospholipid molar ratio is unaffected by hyperthyroidism. The liver mitochondrial phospholipid composition, unlike the microsomal composition, is altered significantly in hyperthyroid rats; a 7.4% phosphatidylcholine decrease is accompanied by a similar additive percentage increase of both phosphatidylethanolamine and cardiolipin. In regard to total phospholipid fatty acid composition in liver microsomes from hyperthyroid rats, no variation has been observed compared with the control rats, whereas in mitochondria from the same animals, a meaningful linoleic acid decrease with a similar arachidonic acid increase has been found. In addition to fatty acid alteration, the separated mitochondrial phospholipid classes also exhibit some increase in stearic acid. Among phospholipids, cardiolipin changes the most of the esterified fatty acids in hyperthyroid rat liver. In this compound, a strong increase in the percentage of both palmitic and stearic acid and a 32.4% decrease of linoleic acid have been found.     

Effects of ethanol on membrane lipids III. Quantitative changes in lipid and fatty acid composition of nonpolar and polar lipids of mouse total liver,mitochondria and microsomes following ethanol feeding

The effects of ethanol on the total, nonpolar, and polar lipids of whole liver, mitochondria, and microsomes have been evaluated. Differences in the fatty acid composition of various lipid subclasses have been compared in control and ethanol treated mice. On the whole polyunsaturated fatty acids, especially arachidonic (20∶4) and docosahexaenoic (22∶6), were found to decrease. The significance of an enzymatic mechanism vs. a peroxidative mechanism to explain the results is discussed. Decreases also were observed in the ratios of arachidonate/linoleate following ethanol feeding. These changes are thought to be associated with decreases in the activity of the chain elongation-desaturation system. The research described herein was conducted while the authors were associated with the University of Detroit, Detroit, Mich. and represents part of the work submitted by J.N. Miceli in partial fulfillment of the requirements for the Ph.D. degree.     

Dietary fats containing concentrates ofcis ortrans octadecenoates and the patterns of polyunsaturated fatty acids of liver phosphatidylcholine and phosphatidylethanolamine

The effects of the mixedcis- 18∶1 isomers and mixedtrans-18∶1 isomers present in partially hydrogenated soybean oil (PHSO) upon the patterns of polyunsaturated fatty acids (PUFA) in liver phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were studied in rats fed concentrates ofcis- 18∶1 ortrans- 18∶1 isomers isolated as triacylglycerides from PHSO. Thecis- 18∶1 andtrans- 18∶1 concentrates were fed at levels equal to those present in PHSO fed at 17.9% of the diet. All diets contained the required amounts of both linoleic and linolenic acids. Thetrans- 18∶1 concentrate was found to suppress the levels of 20∶4ω6 and 20∶3ω9, and to increase the levels of 18∶2ω6 and 20∶5ω3 in PC and PE. Thecis- 18∶1 concentrate suppressed 20∶4ω6 in PC, 20∶5ω3 in PC and PE, and 18∶2ω6 was more effective than thetrans concentrate in suppressing 22∶6ω3. Thetrans- 18∶1 concentrate was more effective in suppressing 20∶4ω6. Thetrans-18∶ isomers appear to modify PUFA metabolism by inhibition of PUFA synthesis, whereas thecis- 18∶1isomers appear to compete with 2-position fatty acyl transfer and to inhibit ω3 PUFA acylation.     

Influence of dietary fatty acids on membrane properties and enzyme activities of liver mitochondria of normal and hypophysectomized rats

Studies are reported on the effects of diets containing fatty supplements with (A) a high concentration of arachidonate (46% concentrate of ethyl arachidonate), (B) a high concentration of linoleate (corn oil), and (C) an essential fatty acid deficient, fully saturated fat (hydrogenated coconut oil) upon lipid composition, membrane permeability, and enzyme activities of liver mitochondria of normal and hypophysectomized rats. The fatty supplements produced differences in the fatty acid composition of the liver mitochondria; hypophysectomy, in addition, influenced the neutral and phospholipid composition. Permeability, indicated by swelling properties, correlated generally with the degree of unsaturation and essential fatty acid content of the lipid of the mitochondria of the normal animals. The fatty supplements also influenced the enzyme acitivites of the mitochondria of the normal animals. The mitochondria of the hypophysectomized animals were less responsive to the differences in the dietary fat in both their swelling properties and enzyme activities. Although the relationship was complex, it appeared that the hypophysis was involved in the functions of essential fatty acids in liver mitochondria.     

Synthesis of phosphatidylcholine and phosphatidylethanolamine at different ages in the rat brain in vitro

The de novo synthesis of choline and ethanolamine phosphoglycerides in brain microsomes from 18 month-old male rats was investigated in vitro by using labeled cytidine-5′-diphosphate choline and cytidine-5′-diphosphate ethanolamine as lipid precursors. The rate of synthesis of the two phospholipid classes was found to be noticeably decreased, as compared to that of adult animals. The addition of exogenous diacyl glycerols to microsomes from ageing rat brain brings the rate of synthesis nearly to the adult levels. The synthesis of choline and ethanolamine phosphoglycerides is not affected in the liver microsomes of ageing rats. The molar distribution of fatty acids in brain microsomal diacyl glycerols of ageing rats is noticeably different from that of adult animals. The content of monoenoic and dienoic species is increased, whereas that of the tetraenoic species is decreased. Base exchange reaction for choline and ethanolamine incorporation into respective phospholipids is not affected in the brain microsomes of the aged rats.     

Transfer of arachidonate from phosphatidylcholine to phosphatidylethanolamine and triacylglycerol in guinea pig alveolar macrophages

Guinea pig alveolar macrophages were labeled by incubation with either arachidonate or linoleate. Arachidonate labeled phosphatidylcholine (PC), phosphatidylethanolamine (PE) and triglycerides (TG) equally well, with each lipid containing about 30% of total cellular radioactivity. In comparison to arachidonate, linoleate was recovered significantly less in PE (7%) and more in TG (47%). To investigate whether redistributions of acyl chains among lipid classes took place, the macrophages were incubated with 1-acyl-2-[1-¹⁴C]arachidonoyl PC or 1-acyl-2-[1-¹⁴C]linoleoyl PC. After harvesting, the cells incubated with 1-acyl-2-[1-¹⁴C]linoleoyl PC contained 86% of the recovered cellular radioactivity in PC, with only small amounts of label being transferred to PE and TG (3 and 6%, respectively). More extensive redistributions were observed with arachidonate-labeled PC. In this case, only 60% of cellular radioactivity was still associated with PC, while 22 and 12%, respectively, had been transferred to PE and TG. Arachidonate transfer from PC to PE was unaffected by an excess of free arachidonate which inhibited this transfer to TG for over 90%, indicating that different mechanisms or arachidonoyl CoA pools were involved in the transfer of arachidonate from PC to PE and TG. Cells prelabeled with 1-acyl-2-[1-¹⁴C]arachidonoyl PC released¹⁴C-label into the medium upon further incubation. This release was slightly stimulated by zymosan and threefold higher in the presence of the Ca²⁺-ionophore A₂₃₁₈₇. Labeling of macrophages with intact phospholipid molecules appears to be a suitable method for studying acyl chain redistribution and release reactions.     

Growth hormone and liver mitochondria: Effects on phospholipid composition and fatty acyl distribution

Effects of growth hormone on phospholipid composition and fatty acyl distribution were studied in liver mitochondria of hypophysectomized rats. After hypophysectomy, only cardiolipin showed a 25% decrease. Its fatty acyl distribution, which consisted mainly of linoleic acid (55–60%) and oleic acid (20%), was unchanged. In phosphatidylcholine and phosphatidylethanolamine fractions the contents of docosahexaenoic and arachidonic acids were decreased with a concomitant increase in linoleic acid content. These changes could be accounted for by small but significant decreases in the activities of Δ⁹-desaturase (sucrose-induced), Δ⁵-desaturase and mitochondrial elongation enzymes. The activities of Δ⁶-desaturase NADH cytochrome b₅ ferri-reductase, cytochrome b₅, NADH cytochrome c reductase and microsomal elongation enzymes remained virtually unchanged. Injection of bovine growth hormone daily for seven days restored cardiolipin and fatty acyl distribution and the enzyme activities. From these and other results, we conclude that growth hormone-dependent increase of respiratory activity of liver mitochondria may be partly mediated by the hormonal effects on membrane lipid distribution.     

Effect of dexamethasone on the fatty acid composition of total liver microsomal lipids and phosphatidylcholine molecular species

Dexamethasone depresses Δ6 and Δ5 and increases Δ9 desaturase and synthase activities. Therefore, we investigated the effect on the fatty acid composition of microsomal liver lipids and phosphatidylcholine (PtdCho) molecular species. After 15 d of treatment we found a notable decrease in arachidonic acid, a small decrease in stearic acid, and increases of linoleic, oleic, palmitoleic, and palmitic acids in liver microsomal total lipids and PtdCho. The study of the distribution of the PtdCho molecular species indicated that 18∶0/20∶4n−6, 16∶0/20∶4n−6, and 16∶0/18∶2n−6 predominated in the control animals. Dexamethasone, as expected because of its depressing effect on arachidonic acid synthesis and activation of oleic and palmitic acid synthesis, evoked a very significant decrease in 18∶0/20∶4n−6 PtdCho (P<0.001) and an important increase in 16∶0/18∶2n−6. The invariability of 16∶0/20∶4n−6 PtdCho could be related to the antagonistic effect of arachidonic and palmitic acid synthesis. PtdCho species containing oleic acid were not significant. The bulk fluidity and dynamic properties of the microsomal lipid bilayer measured by fluorometry using the probes 1,6-diphenyl-1,3,5-hexatriene and 4-trimethylammonium-phenyl-6-phenyl-1,3,5-hexatriene showed no significant modification, probably owing to a compensatory effect of the different molecular species, but changes of particular domains not detected by this technique are possible. However, the extremely sensitive Laurdan detected increased lipid packing in the less-fluid domains of the polar-nonpolar interphase of the bilayer, possibly evoked by the change of molecular species and cholesterol/phospholipid ratio. The most important effect found is the decrease of arachidonic acid pools in liver phospholipids as one of the corresponding causes of dexamethasone-dependent pharmacological effects.     

Effect of diet on choline phosphotransferase,phosphatidylethanolamine methyltransferase and phosphatidyldimethylethanolamine methyltransferase in liver microsomes

Phosphatidylcholine (PC) biosynthesis has been investigated in female rats fed a liquid amino acid, choline-methionine-free diet by assaying in liver microsomes the specific and total activities of choline phosphotransferase, phosphatidyldimethylethanolamine methyltransferase and phosphatidylethanolamine methyltransferase. There was a significant decrease in the specific activity (sp act) of choline phosphotransferase in the liver of rats fed a choline-methionine-free diet. The dietary omission of methionine for 2 wk resulted in a significant decrease in the sp act of choline phosphotransferase. The dietary omission of choline, methionine, B₁₂, folic acid and the addition of a methyl group acceptor, guanidoacetic acid, decreased further the sp act of choline phosphotransferase. The phosphatidyl-ethanolamine methyltransferase sp act increased with the dietary omission of choline and methionine. The dietary omission of choline, methionine, B₁₂, folic acid and the addition of a methyl group acceptor, guanidoacetic acid, resulted in a decrease in the sp act of phosphatidyldimethylethanolamine methyltransferase and an increase in phosphatidylethanolamine methyltransferase. The dietary omission of choline, methionine, B₁₂, folic acid and the addition of a methylation inhibitor, 2-amino-2-methyl-1-propanol, did not result in a significant decrease in the sp act of choline phosphotransferase; however, it did significantly decrease the sp act of phosphatidylethanolamine methyltransferase. The addition of dietary methionine with the inhibitor resulted in a significant decrease in the sp act of the choline phosphotransferase and phosphatidylethanolamine methyltransferase when compared to control and/or when compared to deficient with or without inhibitor. The dietary supply of methionine, as a source of choline, did affect the activity of the enzymes that synthesize PC. The ratio of the substrate, S-adenosylmethionine, and the inhibitory product, S-adenosylhomocysteine, affected the enzymatic activity of phosphatidylethanolamine methyltransferase. It is suggested that the concentrations of these 2 compounds may be important in regulating the methylation of phosphatidylethanolamine in the liver cell.     

Influence of dietary partially hydrogenated vegetable and marine oils on membrane composition and function of liver microsomes and platelets in the rat

The aim of the present study was to investigate the influence of partially hydrogenated vegetable and marine oils on membrane composition and function of liver microsomes and platelets with particular reference to the metabolism of linoleic acid and the production of arachidonic acid metabolites. Four groups of male weanling rats were fed linoleic acid supplemented diets containing 20% (w/w) of partially hydrogenated low erucic acid rapeseed oil (HLRSO), partially hydrogenated herring oil (HHO), olive oil (OO) and trierucin + triolein (TE) for 10 weeks. An additional two groups were fed partially hydrogenated low erucic acid rapeseed oil and partially hydrogenated herring oil without linoleic acid supplementation (HLRSO- and HHO-, respectively). Substantial amounts oftrans fatty acids were incorporated into liver microsomes (12.6% in group HLRSO) and platelets (7.0% in group HLRSO-). This incorporation was not dependent on the dietary linoleic acid level. Hepatic microsomal Δ⁵-desaturase activity was significantly increased after HLRSO feeding compared to OO feeding. Δ⁶-Desaturase activity did not vary in the linoleic acid supplemented groups. Both Δ⁵- and Δ⁶-desaturase activities were significantly increased in groups without linoleic acid supplementation. Docosenoic acid was incorporated into platelet phospholipids in contrast to liver microsomes. In the platelet, docosenoic acid seemed to have a special preference for phosphatidylserine. Very small amounts were incorporated into platelet phosphatidylinositol. Feeding diets HLRSO, HHO and OO did not influence rat platelet cyclooxygenase or 12-lipoxygenase activity. Platelets from rats fed TE, however, produced significantly less 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) than platelets from rats fed OO. Feeding of HLRSO- and HHO- resulted in a significantly diminished production of the arachidonic acid metabolites 12-HETE, 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT) and 6-keto-prostaglandin F_1α in stimulated platelets and aorta. Thus, high dietary levels oftrans isomers of monoenoic acids do not interfere with platelet cyclooxygenase or lipoxygenase activity provided sufficient amounts of linoleic acid are available.     

Fatty acid composition of subcellular particles from sheep platelets and topological distribution of phosphatidylethanolamine fatty acids in the plasma membrane

The fatty acid composition of individual phospholipids in subcellular fractions of sheep platelets and the asymmetrical distribution of phosphatidylethanolamine (PE) fatty acyl chains across the plasma membrane were examined. The main fatty acids of total lipid extracts were oleic (18∶1; 32–41%), linoleic (18∶2, 10–17%), stearic (18∶0; 13–15%), palmitic (16∶0; 11–15%) and arachidonic (20∶4; 8–12%) acids, with a saturated/unsaturated ratio of about 0.4. Each phospholipid class had a distinct fatty acid pattern. Sphingomyelin (SM) showed the highest degree of saturation (50%), with large proportions of behenic (22∶0), 18∶0 and 16∶0 acids. The main fatty acid in PE, phosphatidylserine (PS) and phosphatidylcholine (PC) was 18∶1n−9. Our findings suggest that fatty acids are asymmetrically distributed between thecholineversus the non-choline phospholipids, and also between plasma membranes and intracellular membranes. The transbilayer distribution of PE fatty acids in plasma membranes from non-stimulated sheep platelets was investigated using trinitrobenzenesulfonic acid (TNBS). A significant degree of asymmetry was found, which is a new observation in a non-polar cell. The PE molecules from the inner monolayer contained higher amounts of 18∶2 and significantly less 18∶1 and 20∶5 than those found in the outer monolayer, although no major differences were detected in the transbilayer distribution of total unsaturatedversus saturated PE acyl chains.     

The conversion of phosphatidylethanolamine into phosphatidylcholine labeled in the choline group using methyl lodide, 18-crown-6 and potassium carbonate

A chemical method for the conversion of phosphatidylethanolamine into phosphatidylcholine is described. Methyl iodide in the presence 18-crown-6 (1,4,7,10,13,16-hexaoxacyclooctadecane) and potassium carbonate in benzene is used to alkylate phosphatidylethanolamine in 2.5 hr at 37 C to give an isotopically enriched phosphatidylcholine. The product is purified conventionally and is obtained in 75% yield.     

Changes of fatty acid composition of phospholipids in liver mitochondria and microsomes of the rat during growth

The fatty acid patterns of rat liver mitochondrial and microsomal phospholipids were analyzed from term fetuses, 1 and 4 days old, and adult rats. The main fatty acids of phosphatidylethanolamine and-choline were stearic and palmitic acids, although the patterns differed slightly. The fatty acid composition of corresponding phospholipids in mitochondria and microsomes was similar. The fatty acid pattern of cardiolipin was dominated by linoleic acid. The most consistent feature of the developmental changes in the fatty acid patterns of all phospholipids studied was a decrease in the relative amount of monounsaturated fatty acids. The percentages of saturated fatty acids in phosphatidyl-ethanolamine and-choline increased during neonatal development. It is suggested that the high levels of fetal monounsaturated fatty acids were due to low availability of polyunsaturated fatty acids.     

Dietary fatty acid composition induces comparable changes in cardiolipin fatty acid profile of heart and brain mitochondria

The fatty acid profile of cardiolipin (CL) from brain and cardiac mitochondria was measured to determine whether CL isolated from these two tissue sources responded similarly to alterations in dietary fat composition. Male Wistar rats were fed 20% (w/w) diets containing 2 to 12% (w/w) 18∶2n-6 for four weeks. Despite higher baseline levels of CL 18∶2n-6 in cardiac (54±1% of total fatty acids) compared to brain (13±1%) mitochondria, CL 18∶2n-6 levels increased in proportion to dietary 18∶2 levels. The degree of change in 18∶2n-6 was comparable with both tissues showing an approximate 1.5- to 2-fold increase. The time course of changes in CL fatty acid profile was examined in a subsequent experiment in which animals were fed 20% (w/w) fat diets containing either 3 or 15% α-linoleate. Changes in cardiac CL 18∶1, 18∶2n-6, and 22∶6n-3 levels were observed within one week of feeding. While statistically significant differences were not observed in brain CL until the second week of feeding, the time course did not differ substantively from that observed in heart. The results from this study suggest that while baseline fatty acid profile of cardiac and neural CL differ, mitochondria from both tissues show comparable sensitivity to changes in dietary fat composition. Furthermore, it would appear that the turnover rate of fatty acids in CL is similar in both tissues.     

Hypothyroidism and thyroxin substitution affect the n−3 fatty acid composition of rat liver mitochondria

The effects of hypothyroidism and of daily treatment for up to 21 days with thyroxin (T4, 0.5 μg/100 g body weight) on the fatty acid composition of total lipid, phosphatidylethanolamine, and phosphatidylcholine of rat liver mitochondria were studied. The fatty acid compositions of hypothyroid and euthyroid (control) rats of similar age were compared. The n−6 and n−3 polyunsaturated fatty acids (PUFA) were affected differently by the hypothyroid state. The levels of linoleic (18∶2n−6), γ-linolenic (18∶3n−6) and dihomo-γ-linolenic acids (20∶3n−6) were higher in hypothyroid rats than in controls, while the level of arachidonic acid (20∶4n−6) was lower, which suggests an impairment of the elongase and desaturase activities. The n−3 polyunsaturated fatty acids, eicosapentaenoic (EPA, 20∶5n−3) and docosapentaenoic (22∶5n−3) acids, were higher in hypothyroid rats, whereas the linolenic acid (18∶3n−3) content remained constant. The level of docosahexaenoic acid (DHA, 22∶6n−3) was dramatically decreased in hypothyroid rats, while the levels of C₂₂ n−6 fatty acids were unchanged. The differences were probably due to the competition between n−3 and n−6 PUFA for desaturases, elongases and acyltransferases. When hypothyroid rats were treated with thyroxin, the changes induced by hypothyroidism in the proportions of n−6 fatty acids were rapidly reversed, while the changes in the n−3 fatty acids were only partially reversed. After 21 days of thyroxin treatments, the DHA content was only half as high in hypothyroid rats than in euthyroid rats. These results suggest that the conversion of 18∶2n−6 to 20∶4n−6 is suppressed in the hypothyroid state which favors the transformation of 18∶3n−3 to 20∶5n−3. The marked decrease in DHA content indicates an impairment of the enzymes involved in the DHA metabolism, possibly the n−3 Δ4 desaturase or the acyltransferases. The increased levels of EPA and 22∶5n−3 is consistent with the inhibition of the n−3 pathway at the Δ4 desaturase step. Observed modifications in the fatty acid composition may significantly alter eicosanoid synthesis and membrane functions in hypothyroidism.     

The effect of embryological development on phosphatidylethanolamine methyltransferase,phosphatidyldimethylethanolamine methyltransferase and choline phosphotransferase of rabbit liver microsomes

The effect of embryological development on the two biosynthetic enzymes involved in phosphatidylcholine biosynthesis in liver microsomes of −12, −9, 0, +4, +14, +36 day old rabbits has been determined. The specific activity (pmol phosphatidylcholine formed/min/mg microsomal protein) of the phosphatidyletanolamine methyltransferase in the liver microsomes is very low before birth and a 33% increase at birth occurs when compared to the-12 day old fetal livers. The pmol of phosphatidylcholine formed/min/mg protein by the choline phosphotransferase pathway in fetal liver microsomes is 5, 10, 73, 199, 107 and 307 times greater than by the phosphatidylethanolamine methyltransferase pathway for −12, −9, 0, +4, +14, +36 day old rabbits, respectively. The specific activities of the choline phosphotransferase in the liver microsomes increased from the −12 day old fetal livers to 1.6, 19, 73, 39, 27 times for the −9, 0, +4, +14 and +36 day old animals, respectively. The choline phosphotransferase pathway in comparison to the phosphatidylethanolamine methyltransferase pathway is providing the major phosphatidylcholines in the membranes of the endoplasmic reticulum before birth and early fetal development of the rabbit.     

Influence of elaidate and erucate on heart mitochondria

Male, weanling rats were fed, for up to six weeks, corn oil (CO), rapeseed oil (RSO), partially hydrogenated fat (HF), or a mixture of partially hydrogenated fat and corn oil (HF+CO). The respiratory activity of their isolated heart mitochondria, their hormone-sensitive lipase activity, and the fatty acid compositions of the phospholipids of the mitochondria were determined. The results indicated that heart mitochondria isolated from rats which had been fed corn oil (CO) had a higher rate of oxygen uptake, showed higher respiratory control ratios, higher ADP/0 ratios and a higher rate of ATP synthesis than the heart mitochondria isolated from those fed rapeseed oil or hydrogenated fats. The oxygen uptake rates of the rat heart mitochondria isolated from each dietary group of rats was in order: oleyl carnitine ≫ erucyl carnitine > elaidyl carnitine. The decreased capacity to oxidize substrate by heart mitochondria which had been isolated from the hearts of rats fed rapeseed or hydrogenated soybean oil as compared with those fed corn oil as a sole source of dietary fat seemed related to the mitochondria lipid composition. The type of dietary fat fed had a pronounced influence on the mitochondrial fatty acid compositions of phosphatidylcholine, phosphatidylethanolamine, and cardiolipin. The lipase activity of the RSO-fed group did not show any increment with either epinephrine or supplemental ATP treatment. The substrate preference for lipase activity in myocardium was corn oil-triglycerides > trierucin > trielaidin > tripalmitin. However, cardiac lipid accumulation did not seem related to lipase activity in the myocardium. Taken from a thesis submitted by Chi Ming Lee Hsu in partial fulfillment of the Ph.D. degree in Food Science, University of Illinois at Urbana-Champaign.