Transport form of decanoic acid-1-14C in the lymph during intestinal absorption in the rat.
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Animals↗
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Transport form of 14C-decanoic acid in porta and inferior vena cava blood during absorption in the rat.
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Animals↗
Mutagenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin and perfluoro-n-decanoic acid in L5178Y mouse-lymphoma cells.
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Animals↗
[Decanoic acid, new precursor for in vitro biosynthesis of oleic acid by a plant subcellular fraction].
Various membraneous fractions prepared from a cauliflower homogenate synthesize radioactive oleic acid when they are incubated in a 14C-decanolate solution. The more active fraction is formed of vesicles sedimenting at 30,000 g x 20 mn (heavy microsomes). The labelled precursor is transformed by this fraction mainly into oleic acid and hydroxyacids. ATP, NADPH, CoA and oxygen are required for these reactions. Labelled fatty acids, longer than lauric and (i.e. 14C-myristic, 14C-palmitic and 14C-stearic acids) are not transformed into oleic acid by the subcellular fraction studied in this paper.
Adenosine Triphosphate↗
Effects of perfluoro-n-decanoic acid on the respiratory activity of isolated rat liver mitochondria.
The toxic responses of rats to a single dose of perfluorodecanoic acid (PFDA) include reduced food consumption, severe body weight loss ("wasting syndrome"), and hypothermia. Recent studies have suggested that some of these effects may be due to alterations of basic metabolic processes in animals treated with PFDA. In order to test this hypothesis the effects of PFDA on respiratory activity of isolated rat liver mitochondria were examined. PFDA concentrations up to 87.5 micrograms/ml produced a linear increase in oxygen consumption during state 4 (nonphosphorylating) respiration. This suggested uncoupling of electron transport and oxidative phosphorylation was supported by the observation that PFDA released mitochondrial state 3 respiration from inhibition by oligomycin and stimulated latent ATPase activity. Concentrations of PFDA greater than 87.5 micrograms/ml produced progressively less increase in state 4 oxygen consumption, and a single high concentrations (150 micrograms/ml) completely inhibited state 3 respiration and prevented the uncoupling effect of 2,4-dinitrophenol. These observations suggest that in addition to uncoupling electron transport and oxidative phosphorylation PFDA may affect other energy-transducing functions of liver mitochondria such as inhibiting electron transport. These effects on mitochondrial respiration may help to explain the "wasting syndrome" characteristic of PFDA toxicity.
Animals↗
Mechanism of the serum thyroid hormone lowering effect of perfluoro-n-decanoic acid (PFDA) in rats.
The mechanism and consequences of the serum thyroid hormone lowering effect of perfluorodecanoic acid (PFDA) were examined. Thyroid and pituitary gland functions in PFDA-treated rats were assessed by measuring radioiodine uptake from the circulation and the ability of the thyroid gland to secrete thyroxine (T4) and triiodothyronine (T3) in response to thyrotropin-releasing hormone (TRH) stimulation. Serum levels of reverse triiodothyronine (rT3) were measured to test for possible conversion of T4 to a biologically inactive product and the displacement of radiolabeled T4 from rat albumin in vitro by PFDA was examined. Finally, changes in activity of the thyroid hormone-sensitive liver enzymes glycerophosphate dehydrogenase (GPD) and malic enzyme (ME) in response to PFDA were analyzed. Functional activities of the thyroid and/or pituitary glands appear to be somewhat depressed by PFDA treatment. There was no increased conversion of T4 to rT3. PFDA displaced radiolabeled T4 from rat albumin with an affinity similar to thyroxine. The activities of both GPD and ME were significantly increased in livers from PFDA-treated rats. These results suggest that decreased serum levels of thyroid hormones may be due to (1) reduced responsiveness of the thyroid and/or pituitary glands to hormonal stimulation and (2) a displacement of circulating hormones from plasma protein binding sites by PFDA. Increased activity of the liver enzymes GPD and ME does not reflect the reduction in circulating thyroid hormones and indicates that PFDA-treated rats are apparently not functionally hypothyroid at the tissue level.
Animals↗
Perfluoro-N-decanoic acid effects on enzymes of fatty acid metabolism.
In vitro perfluorodecanoate (PFDA) effects on Pseudomonas acyl-CoA synthetase, Candida acyl-CoA oxidase and pigeon muscle carnitine acetyltransferase were examined. Synthetase made little PFDA-CoA from PFDA. It used palmitate, oleate, laurate and decanoate more extensively. PFDA inhibited acyl-CoA formation from these acids. Palmitoyl-CoA formation was affected most. That of decanoyl-CoA was affected least. Inhibitions appeared to be competitive. Acyl-CoA oxidase test substrates were palmitoyl-CoA, lauroyl-CoA and decanoyl-CoA. Oxidase preferred C-10 and C-12 acyl-CoAs. PFDA inhibited oxidation of C-10 and C-12 acyl-CoAs more than that of palmitoyl-CoA. Inhibitions with C-16 and C-10 acyl-CoAs were competitive, KIs 593 +/- 150 and 76 +/- 6.0 microM. Acetyl-CoA was the best acetyltransferase substrate. C-2 to C-8 transfer from acyl-CoAs was inhibited similarly by PFDA. Inhibitions of C-2 and C-8 transfer were competitive and non-competitive, respectively, KIs 111 +/- 15 and 76 +/- 28 microM.
Animals↗
TPD, FTIR, and Molecular Adsorption Studies of Calcium Hydroxyapatite Surface Modified with Hexanoic and Decanoic Acids.
The surface of synthetic calcium hydroxyapatite Ca10(PO4)6 (OH)2 (CaHAP) particles was modified with hexanoic CH3(CH2)4 COOH (HA) and decanoic CH3(CH2)8COOH (DA) acids in hexane and the resulting materials were characterized by various means. XRD pattern, specific surface area, and morphology of the CaHAP particles were essentially not altered by the modification. FTIR and TPD results indicated that HA and DA molecules are hydrogen-bonded to the surface P-OH groups of CaHAP in three adsorption types. The surface of modified particles became hydrophobic. When the modified samples were outgassed at 500 degrees C, HA and DA were removed and the surface P-OH groups were revived. The modified material adsorbed much less H2O and CO2 than the unmodified one. Copyright 1999 Academic Press.
Journal Article↗
On the biological inactivity of 4,5-dihydroxy-n-decanoic acid-4-lactones.
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4-Butyrolactone↗
Segmentation induced by intraluminal fatty acid in isolated guinea-pig duodenum and jejunum.
Small intestinal movements depend on the composition of the chyme with mixing predominating at high nutrient levels and propulsion being prevalent at low nutrient levels. The mechanisms coupling nutrients to motility are unknown. We used computer analysis of video recordings of isolated guinea-pig duodenum, jejunum and ileum to examine movements induced by a fatty acid, decanoic acid. Increasing intraluminal pressure past a threshold using control saline consistently evoked propulsive reflexes: lumen-occluding constrictions appeared at the oral end propagating at 20.4 +/- 2.4 mm s(-1) (mean +/-s.d., jejunum) to the anal end before being repeated until the intraluminal pressure was returned to control. Subthreshold pressure increases sometimes evoked a transient series of constrictions appearing at the oral end and propagating anally at 18.4 +/- 4.7 mm s(-1) (jejunum). At basal pressures, decanoic acid dose-dependently induced motor activity consisting of 40-60 s episodes of constrictions separated by 40-200 s periods of quiescence and lasting up to 2 h. Five contraction patterns were identified within episodes including localized stationary constrictions; constrictions that propagated slowly (5-8 mm s(-1)) for short distances orally or anally; and constrictions that propagated orally or anally for the length of the preparation at 14-20 mm s(-1). Decanoic acid induced motor activity was reversibly abolished by tetrodotoxin (3 microm), hyoscine (1 microm) and hexamethonium (100 microm), but was insensitive to blockade of P2 purinoceptors by PPADS (60 microm). Thus, decanoic acid induces motor activity equivalent to segmentation in guinea-pig small intestine in vitro and this depends on intrinsic neural pathways.
Animals↗
A two-center study of the development of acute irritation responses to fatty acids.
BACKGROUND: A human 4-hour patch test has been developed for evaluating the acute irritation potential of chemicals. This method was developed for comparative irritation assessments. Although skin irritation responses in human subjects can be quite variable, this test method has proven robust in both intra- and interlaboratory tests. However, the previous interlaboratory studies were not optimal in that slightly differing protocols were used and the studies were not controlled for time of year or source of test chemicals. As a result, some variation in acute irritation responses were seen that might have been reduced somewhat had these variables been controlled to a greater extent. OBJECTIVE: The purpose of the current study was to examine interlaboratory reproducibility of the 4-hour patch test when conducted under as identical as set of test conditions as possible. METHODS: Two laboratories conducted a direct comparison study of the acute irritation potential of three structurally related, undiluted fatty acids (octanoic acid, decanoic acid, and dodecanoic acid) in comparison to a benchmark positive control chemical (20% sodium dodecyl sulfate [SDS]). The studies were run within a 4-month period using the same commercial source of test chemicals. Test subjects were treated with each chemical under occluded patch conditions for gradually increasing exposure duration up to 4 hours. The results were then evaluated in terms of total cumulative incidence of positive responses and time response patterns. RESULTS: Using statistical comparisons of the proportion of the subjects with a positive irritant reaction to each substance, the rank order of irritation potential was decanoic acid >/= octanoic acid > SDS >> and dodecanoic acid. The statistical comparisons and the time-response patterns for each chemical were nearly identical at the two laboratories. There were also very similar, and intriguing, variations in the interchemical response patterns seen in the two studies. CONCLUSION: When conducted under as controlled a set of test conditions as was reasonably possible, this acute irritation protocol shows remarkably high consistency across independent test laboratories, further supporting its continued development and acceptance as a valid and more predictive tool for assessing skin irritation potential.
Adult↗
Origins of the cholesterol in milk.
Studies were conducted to investigate the origin of milk cholesterol in the ruminant. In the first experiment, [1(-14)C]sodium acetate was infused into one side of the udder of a lactating goat via the test canal whereas in the second, (1,2-3H]cholesterol was injected intravenously and concurrently with a [14C]acetate intramammary infusion. In both experiments, blood and milk samples were collected at intervals for 6 days postinjection. Maximum unesterified cholesterol specific activity (sp act) in whole milk appeared at 78 hr after intravenous injections of 3H cholesterol and within 3-7 hr after infusion of [14C]acetate. Virtually all the tritium in milk was associated with unesterified cholesterol. The sp act of 14C-labeled cholesterol was only 20% of gland-synthesized decanoic acid. Decanoic acid is known to be completely synthesized in the mammary gland, and, like cholesterol, acetate is its precursor. The results indicate that, although some milk cholesterol is synthesized in the mammary gland, it is derived principally from serum cholesterol. The data show also that serum cholesterol equilibrates with membrane cholesterol of the lactating cell prior to its secretion in milk.
Acetates↗
Absorption enhancement of rectally infused cefoxitin sodium by medium-chain fatty acids in conscious rats: concentration-effect relationship.
The objective of this study was to assess the relative absorption promoting potency in terms of concentration-effect relationships of the medium-chain fatty acids hexanoic acid, octanoic acid, decanoic acid, and dodecanoic acid in conscious rats, using cefoxitin sodium as the rectally delivered model compound. Rectal uptake of cefoxitin, which was absorbed to a limited extent without enhancer (30 +/- 25%), proved to be significantly enhanced by 2.0 M sodium hexanoate, 0.69 M sodium octanoate, and 0.22 M sodium decanoate, resulting in mean bioavailabilities of 102 +/- 24, 68 +/- 25, and 68 +/- 10%, respectively. Thus, increasing fatty acid chain length results in increased enhancing potency from hexanoic acid to decanoic acid. However, using dodecanoate a statistically significant effect could not be reached, because of its limited aqueous solubility. Optimal chain length for absorption enhancement by medium-chain fatty acids is probably determined by interplay of intrinsic effects on mucosal permeability and solubility of the medium-chain fatty acid.
Administration, Rectal↗
Kinetic studies of the interaction of fatty acids with phosphatidylcholine vesicles (liposomes).
The kinetics of addition of fatty acids (as alkaline solutions of the fatty acid anions) to pre-existing unilamellar phospholipid vesicles (mean diameter 100 nm) has been studied. The phospholipid DMPC (1,2-dimyristoyl-sn-glycero-3-phosphocholine) has been mainly used, together with three fatty acids, oleic acid (cis-9-octadecenoic acid), linoleic acid (cis,cis-9,12-octadecadienoic acid) and capric acid (decanoic acid). Experiments were performed above as well as below the main phase transition temperature (Tm) of DMPC vesicles. The pH chosen to study the fatty acid vesicle interaction (after fatty acid and vesicle mixing) was 8.5 in the case of oleic acid and linoleic acid and 7.4 for capric acid. In the absence of any pre-existing phospholipid vesicles, the addition of alkaline solutions of the fatty acid anions to corresponding buffer solutions of pH 8.5 or 7.4 leads to a partial protonation of the fatty acid anions again resulting in the formation of fatty acid vesicles. This process is rather slow, taking place over a period of hours/days, and the vesicles formed are very polydisperse and include a range of vesicle sizes/shapes. However, in the presence of pre-existing phospholipid vesicles the added fatty acids equilibrate readily within a few minutes and the size of the vesicles that form are then closely related to the size of the originally present phospholipid vesicles; the vesicles formed being generally somewhat larger than the pre-existing vesicles. In the case of the phospholipid DMPC, the mixed fatty acid/phospholipid vesicle system is often formed rather rapidly (particularly above Tm), so that stopped-flow methods have been applied to follow the kinetics of the process. It is proposed that most of the fatty acid molecules are initially rapidly incorporated into the bilayers of the pre-exisiting phospholipid vesicles as monomers, rather than that the added fatty acids form separate fatty acid vesicles. The mean vesicle sizes formed in the systems investigated have been analysed by using dynamic light scattering measurements. The behaviour of the DMPC system was found to be slightly different from the POPC (1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine) system studied before, but the results are consistent with a model that involves growth and subsequent fission of the mixed vesicles. The study provides further support of the "matrix effect" in this type of system [S. Lonchin, P.L. Luisi, P. Walde, B.H. Robinson, J. Phys. Chem. B 103 (1999) 10910-10916]. The pre-existing DMPC vesicles act as a kind of seed to control the behavior of the system in the presence of added fatty acid anions.
Buffers↗
Effects of fatty acids and iontophoresis on the delivery of midodrine hydrochloride and the structure of human skin.
PURPOSE: The purpose of this work was to investigate if fatty acids can increase the iontophoretic delivery of midodrine hydrochloride through human dermatomed skin and to observe the effects of iontophoresis and fatty acids on skin using SEM. METHODS: After prehydration for 1 h, human dermatomed skin was treated with 0-0.3 M fatty acids (oleic acid, linoleic acid, decanoic acid, and lauric acid) in propylene glycol (PG) for 1 h. Then the fatty acid solution was replaced by 1% midodrine hydrochloride aqueous solution, and 0.1 mA/cm2 constant current was applied. Samples were taken over 24 h and analyzed by HPLC. After the treatments outlined above, the epidermis was separated, fixed with glutaraldehyde, and dehydrated for SEM. RESULTS: SEM studies revealed that only 1 h of treatment with fatty acids opened up the tightly compact stratum corneum cell layer, and the permeation study showed a significant increase of the permeability of skin to midodrine hydrochloride after fatty acid treatment. CONCLUSIONS: Using 5% oleic acid pretreatment, with the electrical current offset at 0.1 mA/cm2, the daily delivery of midodrine hydrochloride can provide an adequate clinical application. The enhancement of passive and iontophoretic delivery by fatty acids may be occurring through the same mechanism.
Adjuvants, Pharmaceutic↗
Octanoic acidemia and octanoylcarnitine excretion with dicarboxylic aciduria due to defective oxidation of medium-chain fatty acids.
Five patients aged 7 to 21 months are described who developed attacks of coma after a short prodromal illness with diarrhea or vomiting or both. Four had concomitant hypoglycemia, and all had hypoketonemia, with excessive urinary excretion of medium-chain dicarboxylic acids, medium-chain (omega-1)-hydroxyacids, suberylglycine, hexanoylglycine, and octanoylcarnitine. All patients accumulated octanoic acid, decanoic acid, and cis-4-decenoic acid in plasma. Fibroblasts from three patients showed a decreased rate of octanoate oxidation (10%, 12%, and 29% of control values, respectively). These findings suggest a deficiency of medium-chain acyl-CoA dehydrogenase, most probably an autosomal recessive inherited metabolic disorder. Two of the patients died during an acute attack, and a third had severe neurologic sequelae; the two remaining patients recovered. Plasma free carnitine levels were low, but total carnitine was normal. The three surviving patients underwent a fasting test, which did not lead to hypoglycemia, although hypoketonemia, dicarboxylic aciduria, and excessive mobilization of fatty acids did occur. The surviving patients were maintained on frequent carbohydrate-enriched meals.
Acyl-CoA Dehydrogenases↗
Lipase-catalyzed reactions at different surfaces.
Starting from gold chips, we have tailor-made three surfaces by the self-assembly monolayer technique: one entirely hydrophobic, one hydrophobic with dispersed carboxyl groups, and one hydrophilic, containing hydroxyl groups. Rhizomucor miehei lipase has been adsorbed to the hydrophobic and the hydrophilic surfaces and covalently bound to the surface containing carboxyl groups. The adsorption of two substrates-capric acid (decanoic acid) and monocaprin-on the lipase-covered surfaces was monitored by the surface plasmon resonance (SPR) technique. Biocatalysis was also performed in the SPR instrument by circulating a solution of the substrate, dissolved in an 85:15 water-glycerol mixture at a(w) = 0.81, through the instrument, thus exposing the capric acid or the monocaprin to the lipase-covered surfaces. The product composition was found to depend on the type of surface used. Lipase adsorbed at the hydrophilic surface favored hydrolysis, and capric acid was the main product formed when monocaprin was used as substrate. Lipase adsorbed at a hydrophobic surface and, in particular, lipase covalently bound to a hydrophobic surface favored condensation. More dicaprin than capric acid was formed in experiments with monocaprin as the substrate. Reactions performed outside the SPR instrument showed that small amounts of triglyceride were also formed under these conditions. We believe that this work constitutes the first example of the SPR instrument being used for in-situ biotransformation.
Adsorption↗
Inhibition of energy metabolism in cerebral cortex of young rats by the medium-chain fatty acids accumulating in MCAD deficiency.
Patients affected by medium-chain acyl CoA dehydrogenase (MCAD) deficiency, a frequent inborn error of metabolism, suffer from acute episodes of encephalopathy. However, the mechanisms underlying the neuropathology of this disease are poorly known. In the present study, we investigated the in vitro effect of the medium-chain fatty acids (MCFA), at concentrations varying from 0.01 to 3 mM, accumulating in MCAD deficiency on some parameters of energy metabolism in cerebral cortex of young rats. (14)CO(2) production from [U(14)] glucose, [1-(14)C] acetate and [1,5-(14)C] citrate was evaluated by incubating cerebral cortex homogenates from 30-day-old rats in the absence (controls) or presence of octanoic acid, decanoic acid or cis-4-decenoic acid. OA and DA significantly reduced (14)CO(2) production from acetate by around 30-40%, and from glucose by around 70%. DA significantly reduced (14)CO(2) production from citrate by around 40%, while OA did not affect this parameter. cDA inhibited (14)CO(2) production from all tested substrates by around 30-40%. The activities of the respiratory chain complexes and of creatine kinase were also tested in the presence of DA and cDA. Both metabolites significantly inhibited cytochrome c oxidase activity (by 30%) and complex II-III activity (DA, 25%; cDA, 80%). Furthermore, only cDA inhibited complex II activity (by 30%), while complex I-III and citrate synthase were not affected by these MCFA. On the other hand, only cDA reduced the activity of creatine kinase in total homogenates, as well as in mitochondrial and cytosolic fractions from cerebral cortex (by 50%). The data suggest that the major metabolites which accumulate in MCAD deficiency, with particular emphasis to cDA, compromise brain energy metabolism. We presume that these findings may contribute to the understanding of the pathophysiology of the neurological dysfunction of MCAD deficient patients.
Acetates↗