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At least 19 recordsLinked to original sources

PubMed1986

Role of octanoic and decanoic acids in the control of seizures.

Octanoic and decanoic acid, the major constituents of the Medium Chain Triglyceride (MCT) Emulsion diet, have been detected in appreciable quantities in the peripheral blood of children with intractable seizures treated with the MCT diet. Serum concentrations of these acids as well as beta hydroxybutyrate and acetoacetate rose as the diet was introduced and on full diet showed pronounced diurnal variation and low concentrations in the morning. No correlation between octanoic and decanoic acid concentrations and control of seizures was established, but further studies with octanoic and decanoic acid using animal models are necessary to assess the role of these acids and of control of seizures.

3-Hydroxybutyric Acid↗

PubMed1988

Relative fluorescence of normal and acid lipase-deficient cultured fibroblasts following administration of pyrene decanoic acid.

Skin fibroblasts, derived from normal individuals or patients with Wolman's disease (an autosomal recessive disorder due to acid lysosomal lipase deficiency) were incubated with the fluorescent fatty acid, pyrene-decanoic acid (P10). Measurements of the fluorescence intensities of the total lipid extracts indicated that equal quantities of P10 were incorporated into both cell types. The fluorescence emitted by the intact cells was subsequently recorded in a fluorescence microscope equipped with a microdetector unit, which permitted determination of the fluorescence emitted by the intact cell or by specific regions thereof. The fluorescence intensities emitted by the lipidotic cells exceeded those of their normal counterparts 2- and 5-fold when comparing the entire cells or the perinuclear region, respectively. The cells were then subjected to subcellular fractionation and an analysis of the fractions revealed that up to 85-90% of the fluorescence of the lysosome-mitochondrial pellet was derived from free pyrenedecanoic acid; the latter contributed only 15-18% to the fluorescence of the homogenate or the cytosol. There was no difference in the fluorescence of the lipid extracts from the respective fractions of the lipidotic or normal cells. However, the fluorescence emitted by the intact lysosome-mitochondrial fraction of the lipidotic cells exceeded that of its normal counterpart 2.5-fold. These data suggest that the increased fluorescence intensity of the intact lipidotic cells resulted from a higher quantum yield of free P10 molecules solubilized in the hydrophobic environment of their neutral lipid-containing storage granules.

Cell Compartmentation↗

PubMed1985

Influence of the diet on the portal and lymph transport of decanoic acid in rats. Simultaneous study of its mucosal catabolism.

The absorption route of decanoic acid, a medium chain fatty acid, infused in the intestinal lumen in the presence and absence of long chain fatty acids, has been analyzed. Ex vivo perfusion of isolated intestinal loop and intestinal lymph fistula was the technique used. Decanoic acid infused alone was essentially transported through the portal system. If infused in association with monopalmitin, oleic or palmitic acid, up to 3% of decanoic acid could be diluted in the lymph. Moreover, decanoic acid oxidation by the mucosa increased significantly with palmitic acid and in contrast decreased with oleic acid. These data show that both intestinal absorption processes and mucosal oxidation of the medium chain fatty acids are modulated by the lipid components of the diet.

Animals↗

PubMed1987

The effects of perfluoro-n-decanoic acid (PFDA) on rat heart beta-receptors, adenylate cyclase, and fatty acid composition.

Perfluoro-n-decanoic acid (PFDA) is a member of a family of surfactants with numerous industrial applications. The acute toxicity of PFDA is characterized by body wasting and delayed lethality. Recent reports have indicated that the effects of PFDA may involve an action on the structure of biological membranes which results in an alteration of function. In the present study we extend our work on the membrane actions of PFDA by examining its effects on myocardial beta-adrenoceptor binding characteristics and adenylate cyclase. Following a single injection of PFDA the apparent number of beta-receptor binding sites was reduced compared to pair-fed controls. This change in beta-receptor binding capacity was reflected in a reduced ability of norepinephrine to activate adenylate cyclase. No alterations were observed in basal adenylate cyclase activity or in the ability of NaF or guanylyl imidodiphosphate to stimulate the enzyme. The fatty acid composition of the heart was changed by PFDA treatment. Our results suggest that the toxic effects of PFDA may be due to an alteration of the membrane lipid bilayer leading to changes in the functional activity of myocardial membranes.

Adenylyl Cyclases↗

PubMed1987

Cytotoxic and cytolytic activity of nonadecafluoro-n-decanoic acid on Acholeplasma laidlawii.

We studied the interactions between the perfluorinated fatty acid nonadecafluoro-n-decanoic acid (NDFDA) and the cell wall-less procaryote Acholeplasma laidlawii, which were cultured in an identical medium base but with different serum supplements. When grown in mycoplasma media supplemented with PPLO serum fraction (Difco Laboratories, Detroit, Mich.), A. laidlawii was rapidly killed by low concentrations of toxicant (less than 1.0 mM). At higher concentrations (greater than 10 mM), NDFDA treatment appeared to lyse cells. A. laidlawii cells grown in horse serum-supplemented mycoplasma media were both killed and lysed at the same NDFDA concentration (greater than 10 mM). These data suggest that this perfluorinated fatty acid can be cytotoxic and cytolytic to mycoplasmas. Changes in active concentrations occurred in parallel with changes in growth medium serum supplementation, which is known to alter mycoplasma membrane composition. We propose that NDFDA interacts with the membranes of A. laidlawii cells, resulting in cell death or cell lysis or both.

Acholeplasma laidlawii↗

PubMed1986

Toxic effects of nonadecafluoro-n-decanoic acid in rats.

Nonadecafluoro-n-decanoic acid (ND-FDA) has a single dose ip LD50 of 41 mg/kg and causes anorexia and a wasting syndrome. NDFDA also appears to affect lipid metabolism although the metabolic fate and mechanism of action are not known. Control rats were pair fed with rats given 50 mg/kg. Body weights and food consumption were measured daily; body and organ weights, tissue histopathology, and hematological and clinical chemistry parameters were determined at 4, 8, 12, 16, and 30 days postdosing. Liver samples were obtained for determining cholesterol, cholesterol esters, phospholipids, total lipids, fatty acid ratios, and NDFDA. The rats became anorectic within 4 days and did not resume feeding for 10-12 days, losing about 40% of their body weight. There was a decrease in serum protein; total liver protein decreased and there was an increase in measured fatty acids except for stearic. Liver to body weight ratios of dosed rats were twice those of control rats since absolute liver weights in dosed rats remained constant during the weight loss period. The most striking histopathological change was seen in the liver with a uniform persistent cellular swelling at all times. Separation of the lipids by thin layer chromatography indicated that NDFDA was present in the most polar fraction. There also were fatty changes in the proximal tubular epithelium of the kidneys.

Animals↗

PubMed1989

HPLC analysis of brain and plasma for octanoic and decanoic acids.

Two methods are described for determination of octanoic and decanoic acids in plasma and brain homogenate by "high-performance" liquid chromatography with ultraviolet detection. Analysis of the underivatized acids had a detection limit of only 50 mg/L, but formation of the p-bromophenacyl ester increased the sensitivity by 100-fold, to a detection limit of 0.5 mg/L. The latter procedure gave interassay coefficients of variation of 4.1% and 4.8% for octanoic and decanoic acids, respectively. The corresponding intra-assay values were 3.95% and 4.7% (n = 6). The derivative method, applied to samples of plasma from children receiving a medium-chain triglyceride (MCT) diet, gave values in agreement with results by gas-liquid chromatography. Results have also been obtained for samples from mice, either treated with the medium-chain triglyceride diet or given infusions of sodium octanoate.

Adolescent↗

PubMed1986

The effects of perfluoro-n-decanoic acid in the rat heart.

Perfluoro-n-decanoic acid (PFDA) is a synthetic chemical resembling a 10-carbon fatty acid. Several studies have suggested that the toxic mechanism of PFDA may involve impaired lipid metabolism and/or altered cell membrane function. We examined the possibility that altered cell membrane structure in the heart might lead to changes in the functional activity of the organ. Functional characteristics were determined in the isolated perfused rat heart by measuring the ability of the heart to respond to either sympathetic nerve stimulation or infused norepinephrine. PFDA reduced the intrinsic resting heart rate and the inotropic response to a stimulus with maximal effects occurring 8 days after dosing. In addition, resting heart rate measured in vivo was found to be reduced in PFDA-treated rats 6 to 8 days after dosing. beta-Receptor binding studies conducted 8 days after a single dose of PFDA showed that the maximum binding capacity was reduced by PFDA treatment without significant changes in receptor affinity. It is concluded that the reduction in the inotropic response to catecholamines following PFDA treatment may be explained in part by lower beta-receptor density in the myocardial cell membrane. These effects may be related to the early fall in serum thyroid hormone levels as previously reported.

Animals↗

PubMed1988

Perfluoro-n-decanoic acid: induction of peroxisomal beta-oxidation by a fatty acid with dioxin-like toxicity.

Perfluoro-n-decanoic acid (PFDA) produces toxic effects in rodents similar to those caused by 2,3,7,8-tetrachloro-dibenzo-p-dioxin. A single, intraperitoneal dose (50 mg/kg) of PFDA to Sprague-Dawley rats caused disruption of the endoplasmic reticulum, mitochondrial swelling and increases in intracellular lipid droplets in hepatocytes similar to effects reported previously in dioxin toxicity. PFDA treatment led to large decreases in the activity of plasma membrane alkaline phosphodiesterase and mitochondrial cytochrome c oxidase without affecting lysosomal N-acetyl-beta-glucosaminidase, endoplasmic reticulum NADPH-cytochrome c reductase or peroxisomal catalase activities. PFDA treatment led to moderate peroxisome proliferation and to very large (20-40-fold) increases in the activity of fatty acyl-CoA oxidase, the rate-limiting enzyme in the peroxisomal system of fatty acid beta-oxidation.

Animals↗

PubMed1985

Thyroid, bradycardic and hypothermic effects of perfluoro-n-decanoic acid in rats.

A single ip injection of perfluoro-n-decanoic acid (PFDA) to male Wistar rats resulted in an initially rapid, then gradual decrease in food consumption and a parallel loss of body weight. Body temperatures and resting heart rates were significantly depressed by PFDA treatment. As early as 12 h following a single dose of PFDA, serum thyroxine (T4) levels were significantly reduced and remained depressed throughout the 8 day study. Serum triiodothyronine (T3) was reduced by 35% 12 h following PFDA treatment and remained at that level throughout the study. These preliminary data suggest that an action on the thyroid axis may be an early primary response to PFDA and that some of the observed subsequent effects may in part be secondary to the change in thyroid hormone levels.

Animals↗

PubMed1988

Effect of thyroxine supplementation on the response to perfluoro-n-decanoic acid (PFDA) in rats.

The effects of thyroxine (T4) supplementation on perfluoro-n-decanoic acid- (PFDA) induced decreases in food consumption, body weight, and body temperature were examined. A dose-response study was carried out with 50-, 100-, 200-, or 250-micrograms/kg ip doses of T4 for 7 d prior to PFDA administration, and daily dosing with T4 was continued for an additional 30 d. From this study a T4 dose of 200 micrograms/kg was chosen, and subsequent experiments were conducted with this dose. Supplementation with T4 at 200 micrograms/kg daily alleviated the hypophagia but not the severe weight loss and hypothermia produced by PFDA treatment. Our results suggest that some component of the thyroid axis plays a role in feeding behavior. In addition, the PFDA-induced wasting syndrome and hypothermia appear to be unrelated to changes in serum thyroid hormones. The unexpected observation that severe weight loss occurred in the presence of essentially normal food intake suggests that PFDA alters basic cellular metabolic processes.

Animals↗

PubMed1991

[Effect of inclusion complexation of decanoic acid with alpha-cyclodextrin on rectal absorption of cefmetazole sodium suppository in rabbits].

Inclusion complex of decanoic acid (DA) with alpha-cyclodextrin (alpha-CyD) was prepared as an additive of cefmetazole sodium (CMZ) suppository and rectally administered to rabbits. The resulting complexation was examined by the phase solubility method, differential scanning calorimetry (DSC) and X-ray diffractometry. Plasma concentration and AUC of CMZ after rectal administration of a suppository containing DA/alpha-CyD complex to rabbits increased more significantly than those with none additive.

Adjuvants, Pharmaceutic↗

PubMed1986

The effects of nonadecafluoro-n-decanoic acid on serum retinol and hepatic retinyl palmitate hydrolase activity in male Sprague-Dawley rats.

The effects of nonadecafluoro-n-decanoic acid (NDFDA) on serum retinol levels and hepatic retinyl palmitate hydrolase (RPH) activity were investigated in male Sprague-Dawley rats given a single intraperitoneal (IP) dose of 0, 50, or 100 mg/kg NDFDA and sacrificed at two, eight, or 11 days. Treated animals exhibited depressed serum retinol levels, lymphoid involution, and failure to gain weight in proportion to the dose. Hepatic RPH activities were depressed in both treatment groups at all time points and correlated with serum retinol levels. Hepatic retinol levels were also depressed by Day 11. Extraction of hepatic homogenates with acetone removed NDFDA and increased RPH activities twofold and threefold for the low- and high-dose groups, respectively. Analysis of partially purified RPH showed both NDFDA and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to be noncompetitive inhibitors: KI = 450 and 750 microM, respectively. We conclude that NDFDA causes a decrease in the mobilization of vitamin A from the liver by noncompetitive inhibition of RPH.

Animals↗

PubMed1987

Pathological and hepatic ultrastructural effects of a single dose of perfluoro-n-decanoic acid in the rat, hamster, mouse, and guinea pig.

In rats, the liver is the primary target organ of perfluoro-n-decanoic acid (PFDA) toxicity. Therefore, the effects of PFDA on hepatic ultrastructure were studied in rats. Pathological changes induced by PFDA in hamsters, mice, and guinea pigs were also examined. PFDA caused a severe reduction in body weight in all four species studied. A reduction in food intake was observed in rats and hamsters. However, hamsters continued to consume food at a reduced level, while rats stopped eating for a 5- to 6-day period about 6 days after dosing. The PFDA-induced pathological changes in the hamsters, mice, and guinea pigs resembled those seen in rats to varying degrees. As in the rat, PFDA caused a marked liver enlargement in mice and hamsters and a moderate swelling in guinea pigs. This hepatomegaly was ascribed primarily to individual cell swelling. Thymic atrophy was noted in PFDA-treated hamsters, mice, and guinea pigs. Seminiferous tubular degeneration observed in hamsters and guinea pigs, but not in mice, was not as severe as in the rat, where in some cases frank necrosis has been seen. Ultrastructural changes in the livers of all PFDA-treated animals, regardless of species, included disruption of the rough endoplasmic reticulum, rounding and swelling of the mitochondria with related structural alterations, and mild to extensive proliferation of peroxisomes. This peroxisome proliferative response was greatest in mice and almost absent in guinea pigs. Accumulation of lipid droplets in liver cells due to PFDA treatment was more pronounced in hamsters and guinea pigs than in rats and mice. PFDA-induced hepatomegaly with a concomitant increase in peroxisomes in several rodent species may be associated with an impairment of normal lipid metabolism in the liver by PFDA.

Animals↗

PubMed1989

Modulation of human leukocyte histamine release by sn-1,2-isopropylidene-3-decanoyl-glycerol and decanoic acid cyclopentyl methylester in comparison with effects of synthetic diacylglycerols and a phorbol ester.

Previous studies have shown that the glyceride derivative, sn-1,2-isopropylidene-3-decanoyl-glycerol (IpOCOC9), can trigger human leukocyte histamine release. Approximately 25% of the total cellular histamine content is extruded in the presence of 206 microM of IpOCOC9; at 69 microM, however, the secretagogue action of the compound is marginal. The characteristics of the release induced by IpOCOC9 are closely similar to those reportedly recorded at hyperosmolar triggering of basophils with mannitol, and in many respects they also mimic those observed at phorbol ester-induced histamine release. The compound decanoic acid cyclopentyl methylester (DACPME), a structural analogue of IpOCOC9, fails to induce histamine release. IpOCOC9, but not DACPME, stimulates human polymorphonuclear leukocyte cytosolic Ca2+- and phospholipid-dependent histone III-S kinase activity (unpublished observations). The secretagogue action of IpOCOC9 has therefore tentatively, at least partly, been attributed to a direct protein kinase C activation. In the present studies, we examined the influence of IpOCOC9 and DACPME on histamine release triggered by an ensuing exposure to anti-IgE, the calcium ionophore A23187, formyl-methionyl-leucyl-phenylalanine (FMLP), or 4 beta-phorbol 12-myristate 13-acetate (PMA). It is shown that IpOCOC9-treatment of cells results in either enhancement or reduction of the release induced by anti-IgE or by A23187, whereas FMLP-induced release is consistently reduced and PMA-induced release consistently enhanced by such a treatment. Treatment of cells with DACPME enhances but does not reduce anti-IgE-triggered release, whereas FMLP-induced release is not affected. Pretreatment of the cells with other putative protein kinase C activators like PMA, sn-1-oleoyl-2-acetyl-glycerol (OAG), 1,2-dioctanoyl-glycerol (DiC8) or the glycerol derivative sn-1,2-diacetyl-3-decanoyl-glycerol (DiC2OCOC9) affects secretagogue-induced basophil histamine release according to specific patterns similar to but not identical with those recorded for IpOCOC9 and DACPME. Thus, e.g., DiC2OCOC9 consistently reduces but does not enhance anti-IgE-triggered release. These data show that limited structural changes of IpOCOC9 may qualitatively affect its modulating properties in the human basophil histamine release system.

Calcimycin↗

PubMed1975

[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↗

PubMed1990

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↗

PubMed1989

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↗