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Amniotic fluid lecithin/sphingomyelin ratio, palmitic acid, palmitic acid/stearic acid ratio, total cortisol, creatinine, and percentage of lipid-positive cells in assessment of fetal maturity and fetal pulmonary maturity: a comparison.

Lecithin/sphingomyelin (L/S) ratio, creatinine, percentage of lipid-positive cells, palmitic acid, palmitic acid/stearic acid (P/S) ratio, and total cortisol were analyzed as tests for fetal maturity and fetal pulmonary maturity in 164 samples of amniotic fluid from 121 patients. Fifty samples were taken within 72 hours of delivery. The best tests for fetal maturity (37 weeks) with differential percentages were L/S ratio, palmitic acid, and P/S ratio. In the assessment of fetal pulmonary maturity, we studied an additional 174 samples in which only L/S ratio, creatinine, and lipid-positive cells were analyzed. All tests showed a high predictive value of an immature (positive) result was much less for all six parameters; the three best tests were total cortisol (33%), lipid-positive cells (26%) and L/S ratio (14%).

Amniotic Fluid

Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins.

The effects of lauric acid (C12:0) on plasma lipids and lipoproteins were compared with the effects of palmitic acid (C16:0) and oleic acid (C18:1) in a metabolic-diet study of 14 men by using liquid-formula diets fed for 3 wk each in random order. Lauric acid was supplied in a synthetic high-lauric oil, palmitic acid was provided by palm oil and oleic acid in oleic-rich sunflower seed oil. The high-lauric oil resulted in higher concentrations of plasma total cholesterol (4.94 +/- 0.75 mmol/L [mean +/- SE]) and LDL cholesterol (3.70 +/- 0.57 mmol/L) when compared with high-oleic sunflower oil (4.44 +/- 0.54 and 3.31 +/- 0.44 mmol/L, respectively), but did not raise total and LDL cholesterol concentrations as much as did palm oil (5.17 +/- 0.65 and 3.93 +/- 0.51 mmol/L, respectively). No differences were noted in plasma triglycerides or HDL cholesterol. Lauric acid raises total and LDL cholesterol concentrations compared with oleic acid, but is not as potent for increasing cholesterol concentrations as is palmitic acid.

Adult

Arachidonic and palmitic acid utilization in aged rat brain areas.

We have previously demonstrated that the arachidonic acid (20:4) incorporation into brain lipids differs according to the age of the animals used and the experimental conditions adopted. These differences led to a further investigation of arachidonic acid uptake in both aged and adult rat brains, its transformation into CoA derivatives, its incorporation into diacyl-glycerols and polar lipids, and finally its oxidation to CO2. These metabolic parameters were then compared with those obtained after using the saturated fatty acid palmitate (16:0). In both cases slices or mitochondria from different brain areas of 24-month-old and 4-month-old rats were examined. The results obtained indicate that the uptake of the fatty acids into cells is not modified by age. However, the successive metabolic transformations of the acids are altered to a considerable extent. In particular, in 24-month-old animals (compared with 4-month-old rats) there is a significant decrease of 20:4 in its incorporation into lipids as well as its oxidation to CO2, while arachidonoyl-CoA content increases by about 50%. This increased amount of CoA derivative, which has a potent detergent effect, may interfere with membrane structure and affect membrane physiological functions. Furthermore, because the free arachidonate pool is maintained in a dynamic equilibrium with its esterified forms, the final result may be a perturbation of this equilibrium.

Aging

Modification of the binding of sulphamidochlorobenzoic acid to human albumin by palmitic acid contamination of albumin.

Palmitic acid a common contaminant of albumin preparations, competitively inhibits the binding of sulphamidochlorobenzoicacid (SCBA) to human albumin thus decreasing its observed affinity. The effect of palmitic acid depends on its concentration, i.e. the purity and concentration of the albumin preparation used. The correct value for SCBA affinity was obtained by correcting the experimental data according to the palmitic acid concentration by use of a multiligand analysis method.

Albumins

Synthesis and biologic distribution of mercapto derivatives of palmitic acid.

Mercapto derivatives of palmitic acid are capable of binding 99mTc. Based on the hypothesis that 99mTc-labeled palmitic acid derivatives would behave biologically like palmitic acid and thus could be used as myocardial imaging agents, three mercaptopalmitic acid derivatives have been prepared. The synthesis of 2-mercaptopalmitic acid, 2-mercapto-1,16-hexadecanedioic acid, and 16-mercaptopalmitic acid was accomplished by reaction of the corresponding bromo compound with thiourea. The 35S-labeled compounds and [16-14C]palmitic acid were evaluated in rats with a heat-inflicted myocardial infarction to study the effect of the introduction of the mercapto group. The organ distribution of 2-[35S]mercaptopalmitic acid was most similar to that of [16-14C]palmitic acid.

Animals

Bilayer rigidity of the erythrocyte membrane2H-NMR of a perdeuterated palmitic acid probe.

Perdeuterated palmitic acid was intercalated into the human erythrocyte membrane and its motion studied by dueterium nuclear magnetic resonance (2H-NMR). From analysis of temperature dependent changes in the 2H-NMR spectra and from an analysis of derived moments we conclude that the acyl chains of the erythrocyte lipids do not exhibit a detectable phase transition.

Deuterium

Palmitic acid and lecithin measurements in amniotic fluid.

A method is described for the rapid and quantitative estimation of total amniotic fluid palmitic acid. Palmitic acid and lecithin were measured in 140 samples of amniotic fluid in normal and abnormal pregnancy, and the correlation coefficient between the two parameters was 0.93. It is concluded that amniotic fluid palmitic acid measurements are of value in the prenatal determination of fetal pulmonary maturity.

Amniocentesis

Determination of amniotic fluid palmitic acid concentration for the estimation of fetal lung maturity.

Palmitic acid concentrations in amniotic fluid (AF) were determined in 135 patients with normal and pathological pregnancies between the 27th and 42nd week of gestation. There was a sharp rise in the mean palmitic acid concentration after the 34th weeks of gestation from 2.7 mug/ml to 9.9 mug/ml at term. This increase is almost identical with the rise of AF-lecithin. It was found that between 70% and 100% of AF-palmitic acid originates from lecithin. 65 patients were delivered within 24 h after amniotic fluid sampling. 7 infants of these patients developed a respiratory distress syndrome (RDS). In all cases with RDS AF-palmitic acid concentration was far below 5 mug/ml. Assuming an AF-palmitic acid concentration greater than 5 mug/ml for characterising fetal lung maturity (=no RDS), there were no false negative results, but 16% false positive results. However, the determination of AF-palmitic acid concentration seems to be a most reliable method for the assessment of fetal lung maturity.

Amniotic Fluid

Fetal lung maturity, as assessed by gas-liquid chromatographic determination of phospholipid palmitic acid in amniotic fluid.

We describe a new and specific method for measurement of lecithin palmitic acid in amniotic fluid. Dipalmitoyl lecithin, the major alveolar surfactant, has previously been estimated by measuring the lecithin-sphingomyelin ratio, total lecithin, total phospholipid phosphorus, and (or) total palmitic acid. Our method is more specific for estimation of dipalmitoyl lecithin, because nonphospholipid sources of palmitic acid are removed by solvent extraction. Using a hexane/2-propanol/sulfuric acid system, we obviated the major interferences from triglycerides and free fatty acids. The palmitic acid derived from the phospholipid fraction is measured by gas-liquid chromatography of its methyl ester. No contribution appears to be made by sphingomyelin palmitic acid--probably owing to the mild hydrolysis conditions. The measured palmitic acid therefore appears to be derived from lecithins, principally dipalmitoyl lecithin. The value for palmitic acid determined by this method correlates well with the lecithin-sphingomyelin ratio and total phospholipid phosphorus. Infants are unlikely to develop respiratory distress syndrome when the measured palmitic acid in amniotic fluid exceeds 8.0 mg/liter, which corresponds to an lecithin-sphingomyelin ratio of 2.0.

Amniotic Fluid

[Action of erucic and palmitic acids on rat cardiac myoblasts in primary cell culture. An ultrastructural study (author's transl)].

Primary cultures of beating myocardial cells of neonatal rat are taken in order to observe the ultrastructural modifications caused by certain long chain fatty acids (erucic acid C22 : 1 and palmitic acid C16 : 0). Reference cultures are established and observed at the same time as the others. The eurcic acid create an intense steatosis, on the opposite palmitic acid does not. On the contrary the transormations of certain cellular organites such as mitochondria, dictyosomes, rough endoplasmic reticulum and ribosomes are observed in both cases.

Animals

Palmitic acid activation of peroxidase and its possible significance in mango ripening.

Palmitic acid stimulated the activity of mango peroxidase and reversed the inhibition due to the peroxidase inhibitor present in the preclimacteric fruit. The palmitic acid effect appeared to saturate in the range of 45 to 60 muM palmitic acid. Crude fatty acid extract of the mango exerted similar effect. The percentage stimulation was pH-dependent. Palmitic acid stimulated the enzyme by 18 percent at its optimum pH (5) but the stimulation was in excess of 63 percent at pH 2.5. At pH 2.5 the enzyme concentration versus velocity plot was non-linear and the activation by palmitic acid appeared to saturate between 32 and 48 muM concentration of the effector. The inhibition of the enzyme at and above 0.86 muM concentration of substrate (H202) was not found in the presence of palmitic acid. The effector also changed the heat inactivation kinetics of the enzyme and activated only two out of the four peroxidase isoenzymes present in the climacteric fruit extracts. The results presented indicate the regulatory nature of the enzyme and support its significance in fruit ripening.

Carbon Dioxide

Epithelial-Mesenchymal Transition Shapes the Lipotoxic Response of Colon Cancer Cells to Palmitic Acid.

Saturated fatty acids such as palmitic acid (PA) can induce lipotoxic stress, whereas monounsaturated fatty acids like oleic acid (OA) often promote adaptive responses through lipid droplets (LDs) formation. Here, we reveal that epithelial-mesenchymal transition (EMT) profoundly influences the lipotoxic response of colorectal cancer cells. Using the epithelial-like HCT15 and mesenchymal-like HCT116 cell lines, we combined proteomic, metabolic, and imaging analyses to elucidate how EMT status determines lipid storage capacity and resistance to PA-induced toxicity. A basal proteomic profiling highlighted a striking divergence in metabolic changes: HCT15 cells displayed enhanced glycolysis and reduced expression of LDs biogenesis proteins, while HCT116 cells exhibited oxidative metabolism and a "lipid-rich" proteomic signature enriched in PLIN2, GPAT3, and DGAT1. Functionally, PA triggered massive cytotoxicity and failed to induce LDs in HCT15 cells, correlating with DGAT1/2 downregulation and suppressed triacylglycerol synthesis. In contrast, HCT116 cells showed modest LDs accumulation, preserved mitochondrial function, and strong resistance to lipotoxic stress. OA treatment restored LDs formation and cell viability in both models, underscoring the protective role of unsaturated fatty acids. Notably, forced EMT induction in HCT15 cells by PMA markedly enhanced LDs accumulation and reduced PA-induced death, confirming that EMT confers metabolic plasticity and lipid-buffering capacity. These findings demonstrate that EMT status modulates differential lipid handling and stress adaptation in colon cancer cells, linking mesenchymal transition to enhanced LDs biogenesis and survival under lipotoxic conditions. Data are available via ProteomeXchange with identifier PXD071641.

Humans

Oxidation of [U-14C] palmitic acid by cock spermatozoa.

When washed cock spermatozoa were incubated with [U-14 C] palmitic acid at 37 C for 2 hr under aerobic conditions, radioactivity was recovered as carbon dioxide indicating the fatty acid was oxidized. Little if any radioactivity was recovered as carbon dioxide when spermatozoa were killed by boiling, indicating the necessity for viable spermatozoa for the successful incorporation and oxidation of palmitic acid. To determine whether the oxidation of palmitic acid could serve as a source of energy for cock spermatozoa, ATP concentrations of spermatozoa were compared immediately following ejaculation and after 1,2, and 3 hr of incubation (37 C) with and without the addition of palmitic acid. At 1,2, and 3 hr of incubation, spermatozoa with palmitic acid as a substrate produced significantly (P less than or equal to .03) more ATP (2.62, 2.24, and 1.26 micrograms ATP/10(9) cells, respectively) than did spermatozoa without palmitic acid (1.62, 1.11, and .79 micrograms ATP/10(9) cells, respectively). These findings indicate that palmitic acid, one of the most abundant long-chain saturated fatty acids in cock spermatozoa, can be utilized as a source of energy.

Adenosine Triphosphate

Influence of cicloxilic acid on the intracellular transport of 3H-palmitic acid during acute ethanol fatty liver.

cis-2-Hydroxy-2-phenyl-cyclohexanecarboxilic acid (cicloxilic acid) modifies the rat's hepatocyte intracellular movements of 3H-palmitic acid in the course of fatty liver by acute ethanol intoxication. It counteracts the impairment of radioactive lipid uptake due to ethanol treatment and promotes the early and complete release of the radioisotope inhibited by ethanol. The relevance of these results to the role of changes in the intracellular transport systems in the pathogenesis of ethanol steatosis is discussed. This and previous studies show that cicloxilic acid acts by stimulating the intracellular lipoprotein transport probably preventing by this mechanism the ethanol induced liver injury.

Animals

Effect of dietary palmitic acid on broiler chicks fed on various concentrations of calcium.

1. The effect of dietary palmitic acid on body weight and bone-ash of chicks fed three concentrations of calcium was studied in a 2 X 3 factorial design (0 and 10% palmitic acid, 0.4, 0.7 and 1.0% calcium). 2. Body weight of chick not influenced by the calcium concentration when palmitic acid was not included in the diet. 3. When 10% palmitic acid was included the body weight of chicks fed 0.4 and 0.7% calcium was lower (P less than 0.01) than for the other groups. 4. Bone-ash was lower (P less than 0.01) for chicks fed 0.4% calcium than for the other two calcium concentrations when palmitic acid was not added and palmitic acid at 10% of the diet reduced bone-ash of the chicks fed 0.4 and 0.7% calcium (P less than 0.01).

Animal Feed