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Triglyceride linoleic acid in a fat emulsion for intravenous administration (Intralipid) was used as a marker in an evaluation of fat metabolism in newborn low-birth-weight (LBW) infants. Qualitative data on fatty acids as well as quantification of triglycerides and free fatty acids were obtained by gas-liquid chromatography. Influences on these parameters after a single and after repeated injections of Intralipid revealed differences between low-birth-weight infants appropriate-for-date (AFD) (n=8) and those light-for-date (LFD) (n=5). The LFD exhibited in comparison with the AFD infants an impaired lipolysis of injected triglycerides and a retarded elimination from plasma of released free fatty acids. In LFD, in general, this resulted in triglyceride accumulation and low free fatty acid levels. Heparin facilitated plasma triglyceride lipolysis and free fatty acid elimination from the blood stream.

Investigation of the binding of spin-labeled palmitic acid and its esters with bovine serum albumin is presented. Both probes are shown to bind strictly to strongly and loosely binding centers of protein. The quantitative study allows to determine the binding constant and number of protein binding sites. It is found that the total binding constant for esterified derivative is several times as much as that of palmitic acid.

The dietary intake of essential fatty acids is reflected by the plasma lipid composition. Only scanty data is available on the pattern of plasma fatty acids in young children and the influence of different environments. We analyzed the fatty acid composition of plasma sterolesters, triglycerides, and phospholipids in well-nourished-appearing children from Benin City, Nigeria (n = 8; aged 14.1 +/- 7.2 months) and Düsseldorf, FRG (n = 17; aged 15.2 +/- 5.1 months). The Nigerian group tended to have bigger proportions of the essential omega-6-fatty acids, linoleic acid, and its metabolites, and by far higher values for long-chain omega-3-fatty acids, which are considered to be protective against atherogenesis. The saturated and nonessential monoenoic fatty acids tended to be lower in the Nigerian children, and the ratio of polyunsaturated to saturated fatty acids was higher. We conclude that the quality of dietary fat in the German children was worse and may imply an increased risk for development of atherosclerosis.

Intravenously injected radioactive fatty acids disappear from the circulation at an ever-decreasing rate; about 1% of the injected label remains in plasma for hours. This slow elimination of label can be explained by an extensive recycling of label or by a slows turnover of a portion of the injected label. The results show that a recycling of label can not be responsible for the slow elimination of label, because 1. the specific activities of the tissue fatty acids were much lower than the specific activity of the plasma free fatty acids, and 2. reinjection of the remaining label of 1% into control animals showed the same slow elimination of label. An interpretation of the experiments could be that some fatty acids (about 1%) have a dissociation rate from albumin that is much lower than others, and thus they might be responsible for the late portion of the disappearance curve.

The presence of covalently bound palmitic acid in fibrinogen receptors, glycoproteins (GP) IIb and IIIa, has been explored in human blood platelets. Membrane fractions were isolated from fresh blood platelets labeled with [9,10-3H]palmitic acid and then analyzed for radioactive proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Protein bands were visualized by staining with Coomassie Brilliant Blue, excised, and counted in a liquid scintillation counter. The results indicate that membrane proteins with electrophoretic mobility corresponding to glycoproteins IIb and IIIa incorporate [9,10-3H]palmitic acid. The palmitylated glycoproteins IIb and IIIa were immunoprecipitated by specific anti-GP IIb and GP IIIa antisera. It is interesting to note that the palmitylation of these glycoproteins occurred rapidly in platelets activated with 0.5 unit of thrombin or 30 microM ADP. At the concentration used (100 micrograms/ml), cycloheximide did not inhibit incorporation of [3H]palmitate into the glycoproteins showing that this process is not dependent upon protein synthesis. The acyl moiety was resistant to denaturating detergents, delipidation with organic solvents, and hydrolyzable with hydroxylamine. In the case of membrane protein with the electrophoretic mobility of GP IIb, the radioactive label was significantly decreased after reduction with 2-mercaptoethanol. Final identification of GP IIIa as an acylated product in human platelets incubated with [9,10-3H]palmitic acid was provided by two-dimensional polyacrylamide gel electrophoresis. In contrast to GP IIb alpha, GP IIIa isolated by this method showed the presence of attached radioactive palmitic acid residues. Analysis by high performance liquid chromatography after methanolysis of the [3H]palmitate-labeled glycoproteins confirmed the fatty acid nature of the label. Palmitylation is a newly identified post-translational modification of the fibrinogen receptor which may play an important role in its interaction with the membrane and/or its biological function.

Palmitate, glucose, and glycerol oxidation to CO(2) have been investigated in the fasted state in ten normal subjects and nine patients (six hyperlipoproteinemias, one xanthomatosis, and two glycogenosis) after intravenous injection of [1-(14)C]palmitate, [1-(14)C]glucose, or [1-(14)C]glycerol in tracer amounts. The specific activities and concentrations of plasma palmitate, glycerol, or glucose and expired CO(2) were measured at various intervals after the injection for a period of 24 h. All the studies were analyzed in terms of a multicompartment model describing the structure for each of the subsystems, the transfer of carbon label between subsystems, and the oxidation to CO(2). A bicarbonate subsystem was also included in the model to account for its role in shaping the CO(2) curves. All the CO(2) activity following a palmitate injection could be accounted for by a direct oxidative pathway from plasm FFA with the addition of a 20-min delay compartment. The same also applied to glucose, except that the delay compartment had a mean time of about 150 min. Only about a third of the injected glycerol was directly oxidized to CO(2) from plasma; the delay time was about 4 min. Most of the remainder was converted to glucose. In normals about 45% of the FFA is oxidized to CO(2) directly. This constitutes about 30% of the total CO(2) output. In hyperlipemia the CO(2) output is nearly unchanged and the contribution from FFA is nearly the same. There is a considerable increase (factor of 2), however, in FFA mobilization, most of which is probably diverted to triglyceride synthesis. The glucose and glycerol subsystems are roughly the same in normals and hyperlipemics. About 50% of glucose is oxidized by the direct pathways which accounts for about 35% of the CO(2) output. Glycerol accounts for only 1.5% of the CO(2) produced. Major changes occurred in the glycerol and glucose subsystems in glycogenosis. The changes are consistent with the known deficiency in glucose-6-phosphatase in this disorder. There is a considerable reduction (factor of 2 or more) in the release of glucose to plasma (gluconeogenesis) and in the conversion of glycerol to glucose. Despite the integration of the kinetics of the glucose, glycerol, and FFA subsystems over a 24-h period, 36% of the CO(2) production was still unaccounted for in normals and 50% in hyperlipemics. Thus, some of the carbon must wind up in very slowly turning-over pools which supply CO(2) through subsystems not covered in these studies (triglycerides, glycogen, amino acids, etc.). All the modeling was carried out with the aid of the SAAM25 computer program.

1. Reticulocytosis of 40-50% was obtained in rabbits by daily bleeding. Reticulocytes (plus erythrocytes) were subfractionated into plasma membrane fraction, mitochondria and the post-mitochondrial fraction. 2. In all fractions, fatty acids were incorporated into phospholipids. This process was ATP dependent and represented acylation of lysophospholipids. 3. Incorporation of fatty acids into lysophosphatidic and phosphatidic acids occurred only in the presence of sn-glycerol 3-phosphate and was observed in mitochondria and the post-mitochondrial fraction. It represents a two-step acylation of sn-glycerol 3-phosphate. 4. Incorporation of phosphorylcholine from CDPcholine into phosphatidylcholine was observed in the mitochondrial and the post-mitochondrial fractions. This activity was correlated with NADPH-cytochrome c reductase and was probably connected with the remnants of the endoplasmic reticulum.

A quantitative method for the simultaneous determination of five anticonvulsants in serum has been developed using chemical ionization mass spectrometry without prior chromatographic separation. The technique was shown to be rapid, simple and sensitive, allowing the routine analysis of 50 microliter of serum with good within-day and day-to-day precision.

A method for the determination of free fatty acids in minute serum samples has been developed. The acids are esterified by extractive alkylation, using tetrabutylammonium as a counter ion and pentafluorobenzyl bromide as alkylating reagent. The derivatization of palmitic acid required a reaction time of 25 min. The excess of pentafluorobenzyl bromide is removed by coupling it with a phenoalkylamine and extraction of the product into an acidic aqueous phase. Quantitation is carried out by gas chromatography with electron capture detection. The precision achieved in the determination of 6.2 mug of palmitic acid in 50 mul of mouse serum was 6.1% (S.D.).

Thirty-one children, selected for marked inattention and overactivity, were studied in a double-blind, placebo-controlled crossover study of essential fatty acid (EFA) supplementation. Subjects received the active treatment and placebo conditions for 4 weeks each and were assessed on a variety of cognitive, motor, and standardized rating scale measures. EFA supplementation (evening primrose oil; Efamol) resulted in significantly lower levels of palmitoleic acid (a nonessential fatty acid) and higher concentrations of dihomogammalinolenic acid, an EFA previously found to be deficient in some hyperactive children. Supplementation was also associated with significant changes on two performance tasks and with significant improvement to parent ratings on the subscales designated as Attention Problem and Motor Excess of the Revised Behavior Problem Checklist. However, a variety of eight other psychomotor performance tests and two standardized teacher rating scales failed to indicate treatment effects. When the experiment-wise probability level was set at .05, only 2 of 42 variables showed treatment effects. Baseline EFA concentrations appeared to be unrelated to treatment response. It was concluded that EFA supplementation, as employed here, produces minimal or no improvements in hyperactive children selected without regard to baseline EFA concentrations.

Because of a biological difference between both primary hydroxylgroups of glycerol there are three distinct hydroxylgroups esterified with fatty acids in triglycerides. The distribution of fatty acids in the three distinct positions of triglycerides can be investigated by a combination of partial hydrolysis of triglycerides by pancreatic lipase, phosphorylation of the diglycerides formed and the stereospecific action of phospholipase A on phosphatides. Plasma triglycerides from normal and hyperlipemic humans are analysed. Human plasma triglycerides are highly asymmetric. The 1-position contains more than twice as much palmitic acid as the 3-position. Statistically significant differences are found between normal and hyperlipemic humans for palmitic and linoleic acid at the 2-position, and for oleic and linoleic acid at the 3-position.

21 women who had been followed regularly during their normal pregnancies were examined in the puerperium. The relative fatty acid composition of serum lecithin was analyzed by means of gas-liquid chromatography. Palmitic acid decreased and stearic acid increased, which indicates a shift to more pathway II-synthesized lecithin in the puerperal period. Linoleic acid increased and the longer polyunsaturated fatty acids decreased. These changes were slow as compared to the changes in the saturated fatty acids. No correlations were found between the saturated fatty acids and linoleic acid dominating the polyunsaturated fatty acids. The results indicate different incorporational ways into the lecithin molecule of these fatty acid groups. It is suggested that the deacylation-reacylation cycle is responsible for the high content of longer polyunsaturated fatty acids still 1 week after delivery. 6 weeks after delivery normal values were recorded. Breast-feeding did not seem to influence the fatty acid pattern of serum lecithin.

The percentage fatty-acid composition of the various plasma-lipid fractions from cystic-fibrosis patients with and without pancreatic insufficiency, obligate heterozygotes, and normal subjects was determined. Only the cystic-fibrosis patients with pancreatic insufficiency had significantly abnormal fatty-acid composition. This general observation did not correlate with vitamin-E deficiency, age, sex, or severity of the disease. Thus the altered fatty-acid composition of the different plasma-lipid fractions appears to be a secondary consequence of the pancreatic insufficiency commonly associated with cystic fibrosis and not a direct metabolic defect related to the cystic-fibrosis gene itself.

The study described here makes use of a new technique to assess the level of non-enzymatic glycosylation (glycation) by purified radioactively labelled glucose. Glycation up to 3 molglc/mol protein of human serum albumin, in contrast to previous reports, did not affect the binding of up to 2 mol palmitate, which was reached at a ratio of 7.5 palmitate/HSA. The uptake of palmitate from albumin by either erythrocytes or HL-60 cells also was not influenced by glycation of 3 mol glucose/mol protein. The distribution of palmitate into neutral lipids, phospholipids, or the palmitate designated for oxidation was likewise not influenced. This suggests that levels of albumin glycation likely to be encountered in the blood of diabetic subjects (up to 1 molglc/mol HSA) do not affect fatty acid utilization.

To better characterize essential fatty acid (EFA) deficiency in neonates, we assessed 63 premature infants by serial determinations of plasma fatty acids for the level of linoleic acid, the presence of an abnormal trienoic acid (5,8,11-eicosatrienoic acid [20:3 omega 9]), and the ratio of this compound to arachidonic acid, ie, the triene-tetraene ratio. The data indicated that at age 7 d, 67% of these infants had low plasma linoleic acid levels, 62% showed readily detectable 20:3 omega 9, and 44% had a high triene-tetraene ratio. Infants fed by age 2 d had a normal mean linoleate level at 7 d and none showed detectable 20:3 omega 9 by 10 d. In contrast, infants who were not fed until 7 d showed a very high incidence of abnormal fatty acid status. By maintaining a daily record of linoleate intake, we calculated from regression models that the average amount required to achieve normal fatty acid nutrition was 1.19 g.kg-1.d-1.

We have determined the effect of various rates of glucose infusion on the rates of release of glycerol (Ra glycerol), free fatty acids (Ra FFA), and on energy metabolism in normal human volunteers. Plasma kinetics were determined with use of the stable isotopic tracers D-5-glycerol and [1-13C]palmitate, and energy metabolism was determined by indirect calorimetry. The effect of glucose infusion on Ra glycerol and Ra FFA was dose-dependent. At an infusion rate of 1 mg X kg-1 X min-1, no effect on either kinetic factor was noted. At 4 mg X kg-1 X min-1, both Ra glycerol and Ra FFA were suppressed; at 8 mg X kg-1 X min-1, Ra FFA was even more depressed, but Ra glycerol was similar to the value during the 4 mg X kg-1 X min-1 infusion. At all infusion rates tested, the amount of potential energy available from the sum of the glucose infusion and endogenously mobilized fat was always greater than when no glucose was infused. Glucose decreased fat mobilization by both inhibiting lipolysis and stimulating reesterification, thus causing a significant increase in triglyceride-fatty acid substrate cycling within the adipose tissue.

Phorbol myristate acetate is known to reproduce the stimulated oxidative activities characteristic of phagocytosis and its initial action is on the cell membrane. In the present study the effect of phorbol myristate acetate on the metabolism of the fatty acyl groups of granulocyte phospholipids was examined and compared with that of phagocytic stimuli. Phorbol myristate acetate stimulated the labeling of phosphatidylethanolamine, phosphatidylcholine and phosphatidylinositol by [1-14C]palmitic acid but not by [U-14C]glycerol, whereas starch granules selectively increased the labeling of phosphatidylinositol by both radioactive tracers. Labeled palmitic acid was found at both sn-1- and sn-2-positions of phospholipids and more radioactivity was recovered from the 2-position. The radioactivity at both positions was enhanced in stimulated cells. These data suggest that phorbol myristate acetate increased palmitic acid incorporation into glycerophospholipids by increasing the acylation of the lyso derivatives and that starch granules enhanced the formation of phosphatidylinositol via de novo synthesis and acylation of the lyso derivative as well. Both phorbol myristate acetate and starch granules selectively augmented the incorporation of [1-14C]arachidonic acid into phosphatidylinositol which exhibited the highest specific radioactivity among the phospholipids in control and in stimulated cells. The possible significance of the increased incorporation of arachidonic acid into phosphatidylinositol is discussed.

The incorporation of radiolabeled arachidonic acid and saturated fatty acids into choline-linked phosphoglycerides (PC) of rabbit and human neutrophils was investigated by resolving the individual molecular species by reversed-phase high performance liquid chromatography. PC from neutrophils incubated with a mixture of [3H]arachidonic acid and [14C]stearic or [14C]palmitic acid contains both radiolabels; however, double labeling of individual molecular species is minimal. After labeling for 2 h, the [3H]arachidonate is distributed almost equally between diacyl and 1-O-alkyl-2-acyl species, but it is incorporated into diacyl species containing unlabeled stearate or palmitate at the sn-1 position. In contrast, labeled saturated fatty acids are incorporated only into diacyl species and contain predominantly oleate and linoleate at the sn-2 position. Labeled linoleate is not incorporated into ether-linked species, but is found in the same species as labeled stearate. The findings suggest that mechanisms exist in neutrophils for specific shunting of exogenous arachidonic acid into certain phospholipid molecular species and support the concept that the 1-O-alkyl-2-arachidonoyl species may be a functionally segregated pool of arachidonic acid within the PC of neutrophils.

To determine whether insulin regulation of lipolysis is abnormal in subjects with poorly controlled insulin-dependent diabetes mellitus (IDDM), free-fatty acid flux ([1-14C]palmitate) was measured under conditions ranging from complete insulin withdrawal to hyperinsulinemia. Seven nondiabetic and seven IDDM subjects were studied with the pancreatic clamp technique to control plasma insulin, growth hormone, and glucagon concentrations at the desired levels. Preliminary studies were performed to validate the experimental design. The palmitate flux response to insulin withdrawal (2.5 +/- 0.2 vs. 2.5 +/- 0.2 mumol.kg-1.min-1) and maximally antilipolytic insulin concentrations (0.17 +/- 0.02 vs. 0.23 +/- 0.03 mumol.kg-1.min-1) were not different in nondiabetic and IDDM subjects, respectively. In contrast, IDDM subjects required significantly greater plasma free-insulin concentrations to result in equivalent suppression of palmitate flux compared with nondiabetic subjects. Lipolysis was found to be very sensitive to insulin in nondiabetic humans, with half-maximal suppression occurring at plasma free-insulin concentrations of approximately 12 pM (less than 2 microU/ml). We conclude that adipose tissue lipolysis is normally exquisitely sensitive to insulin and that sensitivity, but not responsiveness to insulin, is impaired in poorly controlled IDDM.

Analysis of the discriminating function was applied to 15 plasma lipid parameters: palmitic, palmitoleic, stearic, oleic and linoleic acids, total NEFA, total lipids, triglycerides, phospholipids, total cholesterol, alpha and beta lipoproteic cholesterol, and lipoproteic alpha: beta, cholesterol: triglycerides and cholesterol: phospholipids ratios, in 84 healthy, normosomic subjects, divided into young, presenile and aged. Highly significant discrimination was obtained between all three groups. The coefficients of discrimination of all the variables employed in individual comparisons are illustrated. A brief account is given of the importance of biohumoral data in the detection of aging, and of the theoretical and practical utility of an investigation of this kind.

The passage of plasma free fatty acids across the pig placenta was investigated in four anaesthetized sows with a total of 41 fetal piglets. The plasma free fatty acid concentrations in fetal piglets were very low and appeared independent of maternal concentrations. In each piglet there was a small positive umbilical venous-arterial concentration difference. There were large differences between the composition of maternal and fetal plasma free fatty acid. The fetal free fatty acid contained relatively large amounts of arachidonic and docosahexaenoic acids. [14C]palmitic acid given intravenously to the sows appeared rapidly in fetal plasma free fatty acids but the amount of radioactivity was low. Analysis of the specific activity of palmitic acid in fetal and maternal blood indicated that little more than 10% of fatty acids coming from the placenta were derived directly from maternal plasma free fatty acids. It is concluded that, in the anaesthetized pig at Caesarean section, fatty acids enter the fetal circulation from the placenta and are taken up by the fetus at rates exceeding the requirements for structure and storage, but the major part of these free fatty acids are not derived directly from maternal free fatty acids.

Gonadotropin-injected pregnant rabbits were delivered by cesarean section near term (30 days after conception (term, 31 days) and 3 1/2 and 4 days post term. Lipid metabolism of the postterm and near-term fetus was compared. Fetal and placental uptake of radioactivity and rate of lipid entry into the fetus, as well as fetal and maternal plasma free fatty acid (FFA) specific activities (at equilibrium) were determined following a single maternal injection of [1-14C]palmitate (50 muCi) administered at cesarean section. Evidence of placental malfunction in the postterm period includes decreased placental uptake and transport of labeled FFA occurring while maternal and fetal FFA dynamics (half times) remain unchanged and a loss in "organization": The strong positive correlation (p less than 0.001) between placental uptake and transfer to the fetus at 30 days' gestation is lost 5 days later. A comparison of maternal and fetal plasma FFA specific activities indicates a substantial (62%) near-term fetal contribution to its own circulating FFA pool. Total plasma FFA is elevated in the postterm fetus concomitant with a decreasing maternal supply. A postterm fetus must therefore contribute lipid from its own reserves (probably liver) in excess of amounts attributed to a near-term fetus, i.e., greater than 62%.

In this study the rate of lipolysis (fatty acid and glycerol release into blood) has been quantified in both normal weight and obese volunteers after both 15 and 87 h of fasting. In each study, the basal rate and subsequent response to epinephrine infusion (0.015 microgram X kg-1 X min-1) were determined. The rate of appearance (Ra) of free fatty acids (FFA) and glycerol were quantified by infusion of [1-13C]palmitate and D-5-glycerol, respectively. Substrate flux rates per unit of body fat mass and lean body mass were calculated from total body water measurements using H2(18)O dilution. In normal volunteers, the basal Ra FFA and Ra glycerol rose markedly with 87 h of fasting, whereas the increases were more modest in the obese subjects. However, the rate of mobilization of fat, in relation to the lean body mass, was higher in the obese subjects than in the normal subjects after 15 h of fasting, and the values were similar in both groups after 87 h of fasting. There was an increased lipolytic response to epinephrine after fasting in both groups. This increased sensitivity may have resulted from the enhancement of fatty acid-triglyceride substrate cycling that occurred after fasting.

The serum fatty acid profiles of patients receiving either intravenous medium or long chain triglycerides were studied. Seventeen hospitalized patients, dependent on total parenteral nutrition, were randomly enrolled into a prospective study. The total parenteral nutrition (TPN) delivered amino acids and glucose and either a 75% medium chain triglyceride and 25% long chain triglyceride (MCT group) physical mixture or all long chain triglyceride (LCT group), as the respective fat sources. The amino acids and glucose were given continuously, and the lipid was given for 10 hours each day over five days. Fatty acid profiles on serum triglycerides and free fatty acids were done in the morning before any lipid was given and also later in the afternoon, near the end of the lipid administration, on days 1, 3 and 5. Medium chain fatty acids rose quickly in the triglyceride fraction in patients given MCT. Rapid MCT hydrolysis occurred as evidenced by the appearance of medium chain fatty acids in the free fatty acid fraction in the afternoon sampling. Clearance of the hydrolyzed medium chain free fatty acids (MCFFA) occurred so that little, if any, were present in the morning sampling one day later. Long chain fatty acids, as either triglycerides or free fatty acids, showed expected increases during the daily infusion, but not of such relative magnitude as the medium chain fatty acids. Medium chain fatty acid incorporation into the phospholipid or cholesterol ester fractions by the end of the five-day feeding period was present but minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Using a constant infusion of [1-14C] palmitic acid into 7 late pregnant guinea-pigs the contribution of circulating maternal lipid to the fetuses was assessed. Within the mother plasma radioactivity was found mainly in free fatty acid with only a small amount circulating as triacylglycerol. In contrast in the fetal plasma [14C] was distributed as one-quarter free fatty acid and three-quarters triacylglycerol, with total [14C] levels being four-fold higher than in the maternal plasma after 160 min of infusion. [14C] Triacylglycerol was found in the fetal liver within 10 min of commencing infusion and levels rose to 12 times the levels of [14C] triacylglycerol in the fetal plasma (per/g or ml) by 100-160 min. [14C] Distribution into the lipid moieties of fetal tissues was found to change with time. By 100-160 min the distribution was: liver, triacylglycerol 83%, phospholipid 7%, free fatty acid 4%; fat, triacylglycerol 80%; heart, triacylglycerol 38%, phospholipid 33%, free fatty acid 9%; kidney, triacylglycerol 15%, phospholipid 58%, free fatty acid 10%; muscle, triacylglycerol 70%, phospholipid 10%, free fatty acid 10%; lung, phospholipid 75%; brain, phospholipid 80%. It was concluded that free fatty acid transferred from the mother contributes substantially to fetal lipids in late gestation in this species.

Dual radiolabel incorporation of [3H]arachidonic acid and [14C]palmitate or [14C]stearate by human neutrophils was employed to study both the release and metabolism of arachidonic acid. Results indicate the involvement of a phospholipase A2 mechanism causing [3H]arachidonate release from membrane phospholipid. Phosphatidylinositol and phosphatidylcholine were the sources of [3H]arachidonate; about twice as much radiolabeled phosphatidylinositol was degraded as phosphatidylcholine. Challenge of neutrophils with opsonized zymosan and calcium ionophores caused the release of [3H]arachidonate; however, ionophores but not opsonized zymosan led to the production of [3H]hydroxyicosatetraenoic acid and [3H]dihydroxyicosatetraenoic acid. These products were preferentially released by neutrophils into the extracellular milieu in contrast with free [3H]arachidonate which remained cell associated. One-third of the [3H]hydroxyicosatetraenoic acid but not [3H]dihydroxyicosatetraenoic acid was reincorporated into cellular lipid, primarily phospholipid. No significant production of [3H]prostaglandin or [3H]thromboxane was detected. In contrast to zymosan and ionophore, phorbol myristate acetate, another potent stimulant of neutrophil oxidative metabolism and degranulation, did not release [3H]arachidonate.

Thirteen infants who received total parenteral nutrition (TPN) in four different ways were studied in order to determine the essential fatty acid (EFA) requirement in pediatric TPN. The serum fatty acid composition of the infants who received fat-free TPN showed EFA deficiency within one week. This deficiency was cured by administering fat emulsion which accounted for 4% of the total caloric content of the infusate. Fat emulsion which accounted for 2% of the total calories neither improved nor prevented EFA deficiency. This means that intravenous fat emulsion, Intralipid, which accounted for 2% of the total calories as linoleic acid, still satisfies the EFA requirement.

Administration of hight doses of retinyl acetate into rats caused an increase in content of retinol in liver tissue and kidney and retinyl palmitate in liver tissue, kidney and blood. The simultaneous administration of thyroxine decreased the accumulation of retinol and retinyl palmitate in liver tissue. At the same time, in kidney content of retinol was increased but content of retinol and retinyl palmitate in blood and retinyl palmitate in kidney did not differ from the values estimated in the control group. The simultaneous administration of retinyl acetate and hydrocortisone decreased the accumulation of retinol and retinyl palmitate in liver tissue, increased the content of vitamin A in blood and did not influence its content in kidney.