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At least 613 records · Page 34Linked to original sources
PubMed1995

In vitro glucuronidation of peroxisomal proliferators: 2-ethylhexanoic acid enantiomers and their structural analogs.

In order to investigate the glucuronidation of 2-ethylhexanoic acid (2-EHA), a metabolite of the plasticizer di-(2-ethylhexyl) adipate, by liver microsomes of several mammalian species including man, a gas chromatography method for the quantification of the corresponding glucuronides was developed. The variation coefficients for intra- and interassay repeatability were less than 3 and 7%, respectively. The rat liver UDP-glucuronosyl-transferase (UGT) presented similar Km and Vmax toward the two enantiomers. The glucuronidation of the racemate 2-EHA or its enantiomers was strongly increased up to six times by treatment of the rats with phenobarbital and, to a lesser extent, by 3-methylcholanthrene. In contrast, the treatment of the rats clofibrate did not modify the activity. The induction was not stereoselective. The Gunn rats, which present a genetic defect in the bilirubin UGT isoforms, were able to glucuronidate the drug as well as the congenic strain. Moreover, the UGT-2B1 isoform, stably expressed in V79 cells, glucuronidated 2-EHA in an appreciable amount. Interspecies comparison indicated that the most active glucuronidation of 2-EHA occurred in the dog and the rat. The lowest activities were observed in the man and the rabbit. In all species considered, except rabbit and guinea pig which glucuronidated the R isomer faster, the R and S enantiomers were glucuronidated to a similar extent. The glucuronidation activity toward compounds chemically related to 2-EHA increased as a function of molecular weight, but was not affected by the position of the methyl or the ethyl moiety on the hydrocarbon chain. A correlation between the glucuronidation rate of 2-EHA and analogs and the activity of PCoA oxidase was observed.

Animals↗
PubMedDate not supplied

Degradation of bis(2-ethylhexyl) phthalate constituents under methanogenic conditions.

The degradation of bis(2-ethylhexyl) phthalate (DEHP) and its intermediary hydrolysis products 2-ethylhexanol (2-EH) and mono(2-ethylhexyl) phthalate (MEHP) was investigated in a methanogenic phthalic acid ester-degrading enrichment culture at 37 degrees C. 2-Ethylhexanoic acid (2-EHA), a plausible degradation product of 2-EH, was also studied. The culture readily degraded 2-EH via 2-EHA to methane which was formed in stoichiometric amounts assuming complete degradation of 2-EH to methane and carbon dioxide. MEHP was degraded to stoichiometric amounts of methane with phthalic acid as a transient intermediate. DEHP remained unaffected throughout the experimental period (330 days).

Biodegradation, Environmental↗
PubMed1986

In vitro responsiveness of ovarian epithelial carcinomas to endocrine therapy.

As previously reported, ovarian epithelial carcinomas may respond to endocrine therapy. We examined the direct effect of progesterone, medroxyprogesteroneacetate, gestoneron, 17-beta-estradiol, tamoxifen, 4-OH-tamoxifen, or N-desmethyltamoxifen on the proliferative capacity of ovarian carcinoma cells by means of the colony assay described by Hamburger and Salmon. The growth rate of 25 tested tumors (ascitic fluid, primary tumor, metastases) was 68%. The plating efficiency was 0.078%. Beside the drug testing estrogen and progesterone receptor levels were determined. The inhibition of colony survival was slightest with 17-beta-estradiol, more pronounced with medroxyprogesteroneacetate, gestoneron, N-desmethyltamoxifen, and progesterone, and greatest with 4-OH-tamoxifen and tamoxifen. Significant and dose-dependent inhibition of greater than 70% was observed with tamoxifen and 4-OH-tamoxifen in 80% of the tested tumors. There was no significant correlation between the in vitro responsiveness and the level of hormonal act not only via an estrogen receptor but also via an antiestrogen-binding site.

Adenocarcinoma↗
PubMed1988

Time-dependent potentiation of insulin release induced by alpha-ketoisocaproate and leucine in rats: possible involvement of phosphoinositide hydrolysis.

The ability of the amino acid leucine and its keto acid, alpha-ketoisocaproate, to induce insulin release, to initiate phosphoinositide hydrolysis, and to amplify the subsequent insulin secretory response to glucose was assessed. In islets whose inositol-containing lipids were prelabelled with myo[2-3H]inositol, the addition of either compound resulted in an increase in insulin output, an increase in 3H efflux, rapid and significant increases in labelled inositol phosphate accumulation and a sustained increase in 3H efflux after removal of the stimulant. Direct measurements of labelled inositol phosphate accumulation in islets previously stimulated with alpha-ketoisocaproate demonstrate that this sustained increase in 3H efflux was the result of a persistent increase in phosphoinositide hydrolysis and was not simply a consequence of the hydrolysis of preformed inositol phosphates into more membrane permeable species. Prior exposure of islets to alpha-ketoisocaproate or leucine also resulted in an amplified secretory response to a subsequent glucose (10 mmol/l) stimulus. While peak first phase insulin release averaged 66 +/- 4 (mean +/- SEM, n = 18) pg.islet-1. min-1 from control islets, this value increased to 204 +/- 14 and 246 +/- 11 pg.islet-1.min-1 in the leucine or alpha-keto-isocaproate pretreated islets respectively. The duration of this amplified response paralleled the duration of the persistent increase in 3H efflux. Prior alpha-ketoisocaproate exposure also amplified the subsequent insulin secretory response to tolbutamide and glyceraldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

2-Ethylhexanoic acid inhibits urea synthesis and stimulates carnitine acetyltransferase activity in rat liver mitochondria.

Adult male 3-month-old Wistar rats were given 0, 100 mg/l, 1, 5 or 10 g/l 2-ethylhexanoic acid in their drinking water for 20 days. Their daily consumption of contaminated water was measured and compared with the free acid found in their 24-h urine samples. The excretion was dose and time dependent. At the termination of the experiment, liver mitochondrial carnitine acetyltransferase activity was induced dose dependently and the citrulline synthesis in the urea cycle inhibited. Our results compare very well with the toxicity of a structural congener of the 2-ethylhexanoic acid, i.e. valproate, an antiepileptic drug.

Acetyltransferases↗
PubMed1990

Evaluation of workers' exposure to 2-ethylhexanoic acid (2-EHA) in Finnish sawmills. A field study.

Exposure to a new wood preservative agent (Sinesto B), whose active ingredient is 2-ethylhexanoic acid (2-EHA), was determined by urinalysis of the parent chemical and its metabolites in workers employed in four Finnish sawmills. The excretion of these chemicals was compared with the inhaled dose analyzed in air samples collected at the breathing zone and with the percutaneous absorption determined by epicutaneous sampling. The main route for entrance of 2-EHA into the body is by breathing, because the urinary concentration of 2-EHA correlated linearly with the concentration of 2-EHA in the air (r = 0.70). There was no correlation between skin contamination and urinary levels of 2-EHA. In most cases the highest urinary concentrations of 2-EHA were found immediately after the work shift. Therefore, in order to evaluate a worker's exposure, the urine sample has to be taken immediately after the work shift. Workers in cranes had the highest exposure to 2-EHA, which describes well the evaporation of Sinesto B into the ambient air. 2-EHA was not found in the urine of non-exposed workers.

Air Pollutants, Occupational↗
PubMed1975

[Studies on the hatching of miracidia of Dicrocoelium dendriticum (author's transl)].

The eggs of Dicrocoelium dendriticum were induced to open by solutions of formic acid and caproic acid (Table 1). The miracidia hatched in O2-free water after the eggs had been dried with N2 or in vacuum. The miracidia were able to live for 3 hours if water contained 20 mM NaCl, 10 mM KCl, and 1 mM CaCl2. Ca++-ions are obviously necessary for the mobility of miracidia. The experimental use of intestinal juice of the Roman snail Helix pomatia gave hatching results which were dependent on the absence of O2 (exposure to N2) and the presence of bacteria with a still unknown function. The dependence on pH seems to be indirect (Abb. 2). Studies on the permeabilities of the egg shell and the embryonic membrane ("vitelline membrane"), the evidence of an oligosaccharide (Abb. 3) liberated from the "spaltraum" (Abb. 1) during egg-opening, and the determination of the osmotic pressure of the hatching process (50% hatching in 1.2--14. Osmols sucrose/1000 ml H2O; Abb. 4) led to the following hypothesis of hatching mechanism: After the activation of the granular gland of the miracidium an enzyme is released into the extra-embryonic "spaltraum". A polysaccharide is digested to an oligosaccharide which cannot permeate the egg shell and the embryonic membrane. The rising osmotic pressure bursts off the operculum.

Animals↗
PubMed1984

Interaction of the mycotoxin penicillic acid with glutathione and rat liver glutathione S-transferases.

The in vitro interaction of the mycotoxin penicillic acid (PA) with rat liver glutathione S-transferase (GST) was studied using reduced glutathione and 1-chloro-2,4-dinitrobenzene as substrates. The inhibition of the GST activity by PA in crude extracts was dose dependent. Each of the different GST isoenzymes was inhibited, albeit at different degrees. Kinetic studies never revealed competitive inhibition kinetics. The conjugation of PA with GSH occurred spontaneously; it was not enzymatically catalyzed by GST, indicating that an epoxide intermediate is not involved in conjugation. The direct binding of PA to GST provides an additional detoxication mechanism.

Animals↗
PubMed1977

Alpha-isopropylmalate synthase from Alcaligenes eutrophus H 16. III. Endproduct inhibition and its relief by valine and isoleucine.

The alpha-isopropylmalate synthase (EC 4.1.3.12) from Alcaligenes eutrophus H 16 was inhibited by L-leucine and alpha-ketoisocaproate. The extent of inhibition was influenced by substrate- and inhibitor concentrations as well as by the pH. Intermediary plateaus, which always appeared in the inhibition curves, suggested cooperative effects. The maximal Hill coefficient was found to be two. At low concentrations of leucine the inhibition mechanism was of the competitive type with respect to substrate acetyl coenzyme A and of the noncompetitive type with respect to substrate alpha-ketoisovalerate. The inhibition was specifically relieved by the addition of valine or isoleucine. The anomalous effect of temperature on enzyme activity was diminished by leucine. The Arrhenius energy of the reaction increased from about 11 kcal/mole in the absence of leucine to about 18 kcal/mole in the presence of leucine. The further addition of valine reversed this effect. The physiological relevance of the alpha-ketoisocaproate-mediated inhibition is discussed.

2-Isopropylmalate Synthase↗
PubMed1985

Severe illness caused by the products of bacterial metabolism in a child with a short gut.

An 8-year-old boy with a short gut had six episodes of metabolic acidosis and neurological dysfunction over a 1 month period. The neurological features consisted of a depressed conscious state, confusion, aggressive behaviour, slurred speech and ataxia. The organic acid profile of urine demonstrated increased amounts of lactic, 3-hydroxypropionic, 3-hydroxyisobutyric, 2-hydroxyisocaproic, phenyllactic, 4-hydroxyphenylacetic and 4-hydroxyphenyllactic acids. Of the lactic acid 99% was D-lactic acid. The anaerobic gut flora consisted almost entirely of Lactobacilli in unusually large numbers. A course of vancomycin prevented further episodes. A urinary organic acid profile may be diagnostic when a person with a short gut develops metabolic acidosis or an unusual encephalopathy and bacterial metabolites should be considered in other patients with unusual combinations of organic acids in the urine.

Acidosis↗
PubMed1975

Effects of alpha-ketomonocarboxylic acids upon insulin secretion and metabolism of isolated pancreatic islets.

In perifused isolated pancreatic islets alpha-ketoisocaproic acid (KIC) or alpha-ketocaproic acid (KC) induced a high insulin secretion rate and a steep increase of the fluorescence of reduced pyridine pyridine nucleotides [NAD(P)H] which fell again to almost prestimulatory levels 6 min after medium change. Insulin release in response to alpha-ketooctanoic (KO) acid started slowly and was accompanied by a decrease of the NAD(P)H-fluorescence trace. Beta-phenylpyruvate which is known to initiate insulin release also caused a fluorescence decrease. Alpha-keto-isovaleric (KIV) acid or pyruvate had no significant effects upon insulin secretion or NAD(P)H-fluorescence. In contrast to l-leucine, l-norleucine or l-valine did not enhance insulin release or fluorescence of NAD(P)H. KIV, alpha-keto-beta-methylvaleric acid (KMV), KIC and KC raised the production their corresponding amino acids by islet cells. From these results it is concluded that alpha-ketomonocarboxylic acids as such trigger insulin release by acting upon receptor sites which differ from those occupied by amino acids.

Amino Acids↗