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PubMed1996

Relationships between bilayer structure and phospholipase A2 activity: interactions among temperature, diacylglycerol, lysolecithin, palmitic acid, and dipalmitoylphosphatidylcholine.

Bilayers composed of phosphatidylcholine initially resist catalysis by phospholipase A2. However, after a latency period, they become susceptible when sufficient reaction products (lysolecithin and fatty acid) accumulate in the membrane. Temperatures near the main bilayer phase transition and saturated long-chain diacylglycerol in the bilayer modulate the effectiveness of the reaction products. The purpose of this study was to identify possible mechanisms for these effects of temperature and diacylglycerol. Various fluorescent probes were used to asses changes in the ability of the reaction products to perturb the bilayer and promote enzyme binding to he membrane surface. Temperature appeared to cause three effects. First, the degree of binding of enzyme at the end of the latency period was greatest near the phase transition temperature where the latency was shortest. Second, the bilayer was more sensitive to perturbation by reaction products near the transition. Third, the disturbance provoked by the products was confined to the membrane surface below the transition but affected deeper regions at higher temperature where the latency period was greater. The latter two effects of temperature required the presence of calcium. Diacylglycerol promoted lateral segregation of reaction products in the bilayer. This effect corresponded with the tendency of diacylglycerol to reduce the length of the latency period at temperature below the phase transition. Therefore, it appeared that temperature affects the latency period by alternating the binding of the enzyme and the depth and magnitude of the bilayer perturbation caused by reaction products. Alternatively, diacylglycerol may enhance the effectiveness of reaction products by inducing them to segregate in the bilayer and thus create local regions of increased impact on the bilayer surface.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2000

Regulation of cholesterol synthesis by oleic and palmitic acid in keratinocytes.

Cholesterol synthesis is essential for homeostasis of the epidermis, being required for both cell division and differentiation, as well as maintenance of the epidermal permeability barrier. Cholesterol synthesis in keratinocytes has been demonstrated to be regulated by sterol levels and the barrier function of the stratum corneum. Cholesterol synthesis in the epidermis is correlated with changes in mRNA levels for key enzymes, such as HMG-CoA synthase and HMG-CoA reductase, which have been previously demonstrated to be coordinately regulated by the sterol regulatory element binding proteins (SREBPs). In this study we demonstrate that a functional sterol regulatory element is required for sterol regulation of HMG-CoA synthase in keratinocytes. We also investigate the regulation of cholesterol synthesis by fatty acids, which are another important constituent of the stratum corneum lipids. Palmitic and oleic acid inhibit 14C-labelled acetate incorporation into sterols in a similar manner to sterols. However, unlike sterols, 50 microM oleic acid increase the steady state mRNA levels of HMG-CoA synthase and the activity of the HMG-CoA synthase promoter. The addition of 50 microM oleic acid to 25-hydroxycholesterol results in an enhancement of the inhibitory effect of the sterol on promoter activity. The inhibition of acetate incorporation into sterols in human keratinocytes by 50 microM palmitic and 50 microM oleic acid is not due to regulation of HMG-CoA synthase at the level of transcription.

Acetates↗
PubMed1996

Effect of butter compared with tallow consumption on postprandial oxidation of myristic and palmitic acids.

To assess the influence of dietary fat composition on rates of oxidation of dietary myristic (MA) and palmitic (PA) acids, eight healthy males consumed prepared solid-food diets for 11 d with 40% of total energy as fat. Fifty-five percent of the energy obtained in the form of fat was provided as butter or beef tallow. On days 8 and 11 of each diet cycle, 20 mg/kg body wt of either [1-(13)C]MA or [1-(13)C]PA was ingested with breakfast. Hourly breath samples were collected over 9 h thereafter and 13CO2 enrichments were determined by using isotope-ratio mass spectrometry. The percentage of [13C]MA appearing in breath carbon dioxide over 9 h was more than twofold that of PA (P < 0.01). Diet fat composition did not influence the mean (+/- SEM) percentage 13C recovered over 9 h from either labeled MA (7.1 +/- 1.0% compared with 8.6 +/- 0.9% for butter and tallow, respectively) or PA (3.3 +/- 0.7% compared with 3.0 +/- 0.9% for butter and tallow, respectively). However, net MA oxidation, calculated as the percent recovery of fatty acids in the meal, was greater (P < 0.05) after the butter (329 +/- 45 mg) than after the tallow (212 +/- 25 mg) breakfast. In contrast, no difference was observed in net oxidation of dietary PA between butter (441 +/- 99 mg) and tallow (348 +/- 95 mg) meals. In conclusion, there was no effect of varying the dietary content of MA and PA on fractional oxidation; consequently, net oxidation of these fatty acids was proportional to their concentration within the diet.

Adult↗
PubMed1994

Protection by vitamin E selenium, trolox C, ascorbic acid palmitate, acetylcysteine, coenzyme Q, beta-carotene, canthaxanthin, and (+)-catechin against oxidative damage to liver slices measured by oxidized heme proteins.

Male SD rats were fed a vitamin E- and selenium-deficient diet, a diet supplemented with vitamin E and selenium, and diets supplemented with vitamin E, selenium, trolox C, ascorbic acid palmitate, acetylcysteine, beta-carotene, canthaxanthin, coenzyme Q0, coenzyme Q10, and (+)-catechin. Liver slices were incubated at 37 degrees C with and without CBrCl3, t-butyl-hydroperoxide, Fe+2, or Cu+2. The effect of antioxidant nutrients on the oxidative damage to rat liver was studied by measurement of the production of oxidized heme proteins (OHP) during the oxidative reactions. Diet supplemented with vitamin E and selenium showed a strong protection against heme protein oxidation compared to the antioxidant-deficient diet. Furthermore, increasing the diversity and quantity of antioxidants in the diets provided significantly more protection.

Acetylcysteine↗
PubMed1989

Glycoprotein Ib and glycoprotein IX in human platelets are acylated with palmitic acid through thioester linkages.

The glycoprotein (GP) Ib-IX complex is a major component of the platelet membrane which mediates adhesion of platelets to exposed subendothelium. GP Ib is a heterodimer with a large alpha chain (Mr = 135,000-145,000) and small beta chain (Mr = 22,000-27,000) linked by a disulfide bond(s). GP Ib is bound in a noncovalent 1:1 complex with GP IX (Mr = 17,000-22,000). We labeled isolated human platelets with [3H] palmitate or surface-labeled platelet membrane glycoproteins with sodium periodate-[3H]sodium borohydride and immunoprecipitated the GP Ib-IX complex from radiolabeled platelet lysates using a mouse monoclonal antibody (SZ.1) which recognizes the intact complex. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography of immunoprecipitates from [3H]palmitate-labeled platelets revealed two radiolabeled bands under reducing conditions at 24 and 19 kDa and two bands under nonreducing conditions at 170 and 19 kDa. As demonstrated by the parallel analysis of immunoprecipitates from periodate-[3H]sodium borohydride-labeled platelets, the [3H]palmitate-labeled bands obtained under reducing conditions corresponded to GP Ib beta and GP IX and the ones obtained under nonreducing conditions to intact GP Ib and GP IX, respectively. Using alkaline methanolysis followed by high pressure liquid chromatography analysis of the methanolysis products, we demonstrated that the radioactivity associated with the GP Ib-IX complex from [3H]palmitate-labeled platelets was, in fact, covalently bound [3H]palmitate in ester linkage to protein. The protein-fatty acid linkage was also disrupted by hydroxylamine at neutral pH. Thus, this study demonstrates that GP Ib beta and GP IX in human platelets are both fatty acid-acylated with palmitate through thioester linkages.

Acylation↗
PubMed1994

Dietary palmitic acid results in lower serum cholesterol than does a lauric-myristic acid combination in normolipemic humans.

In a double-blind crossover study, 17 normocholesterolemic male volunteers were fed carefully designed whole-food diets in which 5% of energy was exchanged between palmitic (16:0) and lauric + myristic acids (12:0 + 14:0) whereas all other fatty acids were held constant. Resident males received each diet during separate 4-wk periods. The test diets supplied approximately 30% of energy as fat and 200 mg cholesterol/d. Compared with the 12:0 + 14:0-rich diet, the 16:0-rich diet produced a 9% lower serum cholesterol concentration, reflected primarily by a lower (11%) low-density-lipoprotein-cholesterol concentration and, to a lesser extent, high-density-lipoprotein cholesterol. No diet-induced changes were noted in the cholesterol content of other lipoproteins, nor did exchange of saturated fatty acids affect the triglyceride concentration in serum or lipoprotein fractions. These data indicate that a dietary 12:0 + 14:0 combination produces a higher serum cholesterol concentration than does 16:0 in healthy normocholesterolemic young men fed a low-cholesterol diet.

Adult↗