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At least 19 recordsLinked to original sources
PubMed1991

The action of 2,3-butane-dionemonoxime on the inotropic state in guinea-pig myocardium.

Isolated papillary muscles from guinea-pig right ventricles were used (temperature 33 degrees C, stimulation frequency 0.5 Hz). Isometric twitch and action potentials were recorded. Upon addition of 2,3-butane-dionemonoxime (BDM) (2 mM) the peak twitch force was reduced from 4.17 +/- 0.4 mN/mm2 to 1.68 +/- 0.3 mN/mm2 (n = 9, P less than 0.001). The time course of the isometric twitch was slightly altered. Time to peak tension (TPT) was reduced by 12.0 +/- 3% (n = 9, P less than 0.001) whereas time to half relaxation (THR) was left unaffected. The rate of rise of force was reduced by 35 +/- 3.2 mN/mm2s i.e. 46 +/- 3%. The action potential duration and amplitude was not significantly changed by the drug. The shape of the curve relating peak twitch force of an extra beat to the preceding test interval, i.e. mechanical restitution, was affected by 2 mM 2,3-butane-dionemonoxime. The curve reached its maximum faster after addition of the drug. Maximum postextrasystolic potentiation (force in response to the prepreceding test interval) was 3.2 +/- 0.4 mN/mm2 in 2 mM 2,3-butane-dionemonoxine and 7.6 +/- 0.7 mN/mm2 in control (n = 6). However the percentage potentiation was very similar in control (82%) and in presence of 2,3-butane-dionemonoxime (91%). Peak twitch force in relation to peak force of the preceding potentiated contraction during decay of postextrasystolic potentiation was analysed. There was a linear relation between the variables, the slope being 0.34 +/- 0.04 in control and 0.30 +/- 0.02 in 2,3-butane-dionemonoxime. This suggests that the drug is without an action on the fraction of calcium recirculating within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1975

A study of the oxidation of butan-1-ol and propan-2-ol by nicotinamide-adenine dinucleotide catalysed by yeast alcohol dehydrogenase.

1. The kinetics of oxidation of butan-1-ol and propan-2-ol by NAD+, catalysed by yeast alcohol dehydrogenase, were studied at 25 degrees C from pH 5.5 to 10, and at pH 7.05 from 14 degrees to 44 degrees C, 2. Under all conditions studied the results are consistent with a mechanism whereby some dissociation of coenzyme from the active enzyme-NAD+-alcohol ternary complexes occurs, and the mechanism is therefore not strictly compulsory order. 3. A primary 2H isotopic effect on the maximum rates of oxidation of [1-2H2]butan-1-ol and [2H7]propan-2-ol was found at 25 degrees C over the pH range 5.5-10. Further, in stopped-flow experiments at pH 7.05 and 25 degrees C, there was no transient formation of NADH in the oxidation of butan-1-ol and propan-2-ol. The principal rate-limiting step in the oxidation of dependence on pH of the maximum rates of oxidation of butan-1-ol and propan-2-ol is consisten with the possibility that histidine and cysteine residues may affect or control catalysis.

1-Propanol↗
PubMed1978

4-(6-Methoxy-2-naphthyl)butan-2-one and related analogues, a novel structural class of antiinflammatory compounds.

A series of compounds related to 4-(6-methoxy-2-naphthyl)butan-2-one has been prepared and tested for antiinflammatory activity by the cotton pellet granuloma method. Compounds possessing a small lipophilic group such as methoxyl, methyl, or chloro in the 6 position in conjunction with a butan-2-one side chain in the 2 position of the naphthalene ring were most active. The indtroduction of a methyl group along the side chain was invariably deleterious. Good activity was generally retained by forming esters of a butan-2-ol side chain.

Animals↗
PubMed1991

The response of evidential breath alcohol testing instruments with subjects exposed to organic solvents and gases. I. Toluene, 1,1,1-trichloroethane and butane.

Experimental work has been undertaken to investigate the potential interference of toluene, 1,1,1-trichloroethane and butane with the evidential breath alcohol testing instruments used in Great Britain (Lion Intoximeter 3000 and Camic Breath Analyser). Volunteers inhaled the volatile substances in an exposure chamber for up to 4 hours, at concentrations of 100, 350 and 600ppm respectively. Subsequently breath was tested on leaving the chamber. No interference was observed with the breath alcohol instruments when the subjects were exposed to toluene and 1,1,1-trichloroethane. A short-term response immediately after exposure was observed for subjects exposed to butane. Further analytical work involving blood and breath samples demonstrated that all three volatile substances were absorbed during exposure and were detectable in blood for at least 3 hours post-exposure. Their elimination post-exposure followed an exponential decay.

Adult↗
PubMed1979

[Experimental poisoning with gaseous hydrocarbons: changes in concentrations of propane and butane in the lung and adipose tissue in relation to the time of death].

Postmortal changes of propane, butane and iso-butane concentration in the lung and fat of mice exposed to lethal intoxication with commercial liquid gas are studied. The hydrocarbon tissue concentrations after exposure were determined by gas liquid chromatography. The hydrocarbons progressively decreased in the lung and disappeared, depending on the degree of putrefaction; even in case of remarkable putrefaction, it was still possible to detect them in the fat tissue.

Adipose Tissue↗
PubMed1978

Potential bis-alkylating agents for cancer chemotherapy. Approaches to the synthesis of 2-sulfonyl-1,4-bis(methanesulfonoxy)butanes.

Three general methods for the synthesis of derivatives of the bis-alkylating agent, myleran [1,4-bis(methane-sulfonoxy)butane (1)], are presented. These derivatives contain a lipophilic group attached to the 2 position of 1,4-bis(methanesulfonoxy)butane by means of a sulfonyl function. As examples of the scope of the methods, the synthesis of seven such derivatives (12a-g) is presented. All seven were inactive against L1210 and P388 leukemia in the mouse.

Alkylating Agents↗
PubMed1978

Inactivation of glutamate dehydrogenase and glutamate synthase from Bacillus megaterium by phenylglyoxal, butane-2,3-dione and pyridoxal 5'-phosphate.

Reaction of phenylglyoxal with glutamate dehydrogenase (EC 1.4.1.4), but not with glutamate synthase (EC 2.6.1.53), from Bacillus megaterium resulted in complete loss of enzyme activity. NADPH alone or together with 2-oxoglutarate provided substantial protection from inactivation by phenylglyoxal. Some 2mol of [14C]Phenylglyoxal was incorporated/mol of subunit of glutamate dehydrogenase. Addition of 1mM-NADPH decreased incorporation by 0.7mol. The Ki for phenylglyoxal was 6.7mM and Ks for competition with NADPH was 0.5mM. Complete inactivation of glutamate dehydrogenase by butane-2,3-dione was estimated by extrapolation to result from the loss of 3 of the 19 arginine residues/subunit. NADPH, but not NADH, provided almost complete protection against inactivation. Butane-2,3-dione had only a slight inactivating effect on glutamate synthase. The data suggest that an essential arginine residue may be involved in the binding of NADPH to glutamate dehydrogenase. The enzymes were inactivated by pyridoxal 5'-phosphate and this inactivation increased 3--4-fold in the borate buffer. NADPH completely prevented inactivation by pyridoxal 5'-phosphate.

Aldehydes↗
PubMed1977

Behavioral comparisons of R-2-amino-1-(2,5-dimethoxy-4-methylphenyl) butane (BL-3912A) with R-DOM and S-amphetamine.

The behavioral effects of R-2-amino-1-(2,5-dimethoxy-4-methylphenyl) butane or BL-3912A were compared with those of S-Amphetamine and R-DOM. BL-3912A facilitated acquisition of shuttle box responding by rats without increasing noncontingent intertrial (ITI) activity, while S-Amphetamine increased both avoidance and ITI responding. R-DOM had a biphasic effect on avoidance responding, increasing it at low doses and disrupting at higher doses. At doses that facilitated shuttle box responding, BL-3912A had no effect on unacclimated motor activity of rats nor on the rate of continuous avoidance responding by rats. S-Amphetamine increased the frequency of both motor activity and operant avoidance responding, while R-DOM decreased motor activity and increased operant avoidance responding. By facilitating avoidance behavior without increasing othermeasures of psychomotor activity, BL-3912A represents a unique psychopharmacological agent clearly different from R-DOM and S-Amphetamine.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1976

On the reaction kinetics in water of 1,3-propane sultone and 1,4-butane sultone: a comparison of reaction rates and mutagenic activities of some alkylating agents.

To determine correlations between the biological action pattern and chemical reactivity of alkylating agents, the rate constants for reactions of 1,3-propane sultone and 1,4-butane sultone with a series of nucleophiles at 37 degrees C have been determined. Previously published data on the mutagenicity of the two sultones and of some alkyl methanesulfonates and dialkyl sulfates towards Schizosaccharomyces pombe have been used in the evaluation of the dependence of mutagenic effectiveness on chemical reactivity. It is of interest to note that the mutagenic effectiveness of the two sultones, if expressed per alkylating event at a certain low nucleophilicity is the same as that of e.g. methyl methanesulfonate and ethyl methanesulfonate.

Alkanesulfonates↗
PubMed1990

Cytotoxicity, sister-chromatid exchanges and DNA single-strand breaks induced by 4-oxo-4-(3-pyridyl)butanal, a metabolite of a tobacco-specific N-nitrosamine.

The tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is metabolized by alpha-carbon hydroxylation to reactive diazohydroxides and aldehydes. The aim of this study was to determine the relative ability of one NNK-derived aldehyde, 4-oxo-4-(3-pyridyl)butanal, to induce cytotoxicity, sister-chromatid exchanges (SCEs) and DNA single-strand breaks (SSBs) in V79 cells. Our data demonstrate that this aldehyde is cytotoxic for V79 cells (IC50 = 0.4 mM) and induces SCEs at concentrations ranging from 0.01 to 0.5 mM. DNA SSBs were observed at concentrations ranging from 0.05 to 1 mM and were repaired within 8 h. When V79 cells were cultured with primary hepatocytes, there was a reduction in the frequency of SCEs induced by the aldehyde. This suggests that hepatocytes can partially deactivate the aldehyde. Our results suggest that this aldehyde is one of the reactive intermediates generated during NNK metabolism.

Animals↗
PubMed1992

Determination of nickel in biological materials after microwave dissolution using inductively coupled plasma atomic emission spectrometry with prior extraction into butan-1-ol.

A sensitive procedure has been developed for the determination of ultratrace amounts of nickel in biological materials by inductively coupled plasma atomic emission spectrometry after extraction of the nickel ion into butan-1-ol by using 1,5-bis(di-2-pyridylmethylene)thiocarbonohydrazide as the extracting reagent. Fast, efficient and complete sample digestion is achieved by an HNO3-HCl poly(tetrafluoroethylene) bomb dissolution technique using microwave heating. Results obtained for eleven certified reference materials agreed with the certified values.

Animals↗
PubMed1991

Comparison of DNA alkali-labile sites induced by 4-(methylnitrosamino)-1(3-pyridyl)-1-butanone and 4-oxo-4-(3-pyridyl)butanal in rat hepatocytes.

4-Oxo-4-(3-pyridyl)butanal (OPB) is an aldehyde formed during the activation of the tobacco-specific N-nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Using the DNA alkaline elution technique, the properties of DNA alkali-labile sites induced in the isolated rat hepatocytes by NNK and OPB were compared. The DNA single-strand break (SSB) frequencies in vitro, as measured by the elution rate (ER), ranged from 0.015 to 0.479 and were proportional (r2 = 0.991) to the dose (0-2 mM) of OPB. These concentrations, however, were slightly cytotoxic. For example, the LC50 after 4 h of exposure was 2.8 mM. This suggests that OPB-induced DNA SSB result from additive effects of OPB-DNA interaction and the indirect DNA damage associated with OPB cytotoxicity. NNK induced a significant and dose-dependent increase of DNA fragmentation at concentrations ranging from 0.5 to 5.0 mM with ER values ranging from 0.012 to 0.274 (r2 = 0.951). Genotoxicity as measured by the DNA-damaging potency coefficient (DDP) was 810, 345, 131 and 75 for N-methyl-N-nitrosourea (MNU), N-nitrosodimethylamine (NDMA), OPB and NNK respectively. Both MNU- and NNK-induced DNA lesions showed increased lability with increased pH (from 12.1 to 12.5) of the eluting buffer (r2 = 0.979 and 0.967 respectively). In contrast, the number of OPB-induced labile sites were not affected by increases in the pH. These results indicate that OPB is not the metabolite contributing the majority of alkali-labile sites generated by NNK. The filter elution procedure was used to study the in vitro rejoining of SSB in DNA induced by NNK. The extent of DNA SSB rejoining after 18 h of culture of hepatocytes in NNK-free medium were dependent on the concentration of NNK (0.5, 2.0 and 5.0 mM) and ranged from 50 to 90%. Rats were injected s.c. with NNK (0.39 mmol/kg). SSB frequency in liver DNA increased rapidly and reached a maximum 12 h after injection. DNA SSB frequency declined during the next 2 weeks with biphasic kinetics. The fast phase (75% rejoining of DNA SSB between 12 h and 2 days) was followed by a slow one (25% of DNA SSB maintained during the next 5 days but not present after 2 weeks). The results of this study better define the role of OPB-induced DNA damage. The persistence of DNA SSB in the liver of NNK-treated rats reflects the inability of this tissue to repair all DNA lesions.

Analysis of Variance↗
PubMed1992

Species differences in urinary butadiene metabolites; identification of 1,2-dihydroxy-4-(N-acetylcysteinyl)butane, a novel metabolite of butadiene.

1,3-Butadiene (BD) is used in the manufacture of styrene-BD and polybutadiene rubber. Differences seen in chronic toxicity studies in the susceptibility of B6C3F1 mice and Sprague-Dawley rats to BD raise the question of how to use the rodent toxicology data to predict the health risk of BD in humans. The purpose of this study was to determine if there are species differences in the metabolism of BD to urinary metabolites that might help to explain the differences in the toxicity of BD. The major urinary metabolites of BD in F344/N rats, Sprague-Dawley rats, B6C3F1 mice, Syrian hamsters, and cynomolgus monkeys were identified as 1,2-dihydroxy-4-(N-acetylcysteinyl)-butane (I) and the N-acetylcysteine conjugate of BD monoxide [1-hydroxy-2-(N-acetylcysteinyl)-3-butene] (II). These mercapturic acids are formed by addition of glutathione at either the double bond (I) or the epoxide (II) respectively. When exposed to approximately 8000 p.p.m. of BD for 2 h, the mice excreted 3-4 times as much metabolite II as I, the hamster and the rats produced approximately 1.5 times as much metabolite II as I, while the monkeys produced primarily metabolite I. The ratio of formation of metabolite I to the total formation of the two mercapturic acids correlated well with the known hepatic epoxide hydrolase activity in the different species. These data suggest that (i) the availability of the monoepoxide for conjugation with glutathione is highest in the mouse, followed by the hamster and the rat, and is lowest in the monkey; and (ii) the epoxide availability is inversely related to the hepatic activity of epoxide hydrolase, the enzyme that removes the epoxide by hydrolysis. The ratio of the two mercapturic acids in human urine following BD exposure may indicate the pathways of BD metabolism in humans and may aid in the determination of the most appropriate animal model for BD toxicity.

Acetylcysteine↗
PubMed1977

The metabolism of the neuroleptic agent 1 (4'-fluorophenyl)-4-(cyclohexyl-1'-piperzinyl-4'-carboxylated)-butan-1-one hydrochloride in rats and man.

1. An oral dose the neuroleptic agent 1-(4'-fluorophenyl)-4-(cyclohexyl-1'-(14C)piperazinyl-4'-carboxylate)butan-1-one was mainly eliminated in the urine within 12 h by rats and man. During 5 days, 63-6% and 83-3% was eliminated in the urine of rats and man respectively. 2. Plasma concentrations in man related a maximum during 30 min to 1 h, representing 1-43 microgram equiv./ml. The proportion of unchanged drug in plasma decreased from 48% at 15 min to less than 10% after 1 h. 3. Seven major radioactive components were detected in the chloroform extract of basified rat urine and five major components in similar extracts of human urine. The major rat metabolites were isolated and identified by mass spectrometry as components resulting from mono- and dihydroxylation in the cyclohexane ring, reduction of the keto group to a secondary alcohol and hydrolysis and decarboxylation of the cyclohexylcarbamoyl group. The major metabolite in the rat urine extract was the dihydroxylated secondary alcohol derivative while the major human metabolite was the monohydroxylated secondary alcohol derivative. The metabolites were also partly eliminated as conjugates.

Administration, Oral↗
PubMed1991

Synthesis and immunopharmacological analysis of selected butanic and butanodionic acid amides containing aziridine unit. II.

In the reaction of butanic and butanodionic acid chlorides with amines, amides 1-10 were produced. Addition of aziridine to a double bonds was performed in alkaline medium which resulted in aziridine derivatives of both acids. Pharmacological study revealed that the preparations examined possess immunotropic, strongly suppressive activity (PFC, E-RFC), partly IgG level; they leave the titer of circulating IgM unchanged. It seems that rather the basic system of acids than the substituents introduced to it are responsible for the effect of the compounds.

Animals↗
PubMed1978

Clinical and metabolic consequences to cattle of rumen overdosing with di-ureido iso-butane (DUIB).

Di-ureido iso-butane (DUIB) was overdosed on three occasions to two year-old bullocks, under experimental conditions. Six g/kg live weight of DUIB was mixed manually into the rumen contents formed by a predominantly hay diet (10 kg) with added concentrates (2 kg). Marked clinical signs were observed for 72 h before recovery. Food and water intake were interrupted and a smell of ammonia saturated the accommodation. Blood concentrations of urea-nitrogen increased, while glucose fell; a metabolic alkalosis was present. Rumen VFA concentrations fell, but without altering the proportions of the individual acids present, pH increased, urea-nitrogen and ammonia-nitrogen concentrations fluctuated markedly. The pH of duodenal contents increased. Clinical recovery appeared complete after six days with biochemical homeostasis nearly restored.

Ammonia↗
PubMedDate not supplied

Platelet aggregation and adhesiveness as well as blood lipids level in dogs treated with di-(1-isoquinolinyl)-di-(pyridyl-2')-butane and carbocromen.

The effect of di-(1-isoquinolinyl)-di-(pyridyl-2')-butane (S-147) on platelet aggregation and adhesiveness as well as on blood lipids level (total lipids, triglycerides, total cholesterol) was tested in mongrel dogs, in comparison with carbocromen. The compounds administered iv (2 mg/kg/day) over 7 days inhibited ADP-induced aggregation, being without depressive influence on platelet adhesiveness. S-147 exhibited slightly stronger effect than carbocromen. The inhibition of platelet aggregation was accompanied by the decrease of serum lipids level.

Animals↗
PubMed1976

Comparison of the effects of R-(-)-2-amino-1-(2,5-dimethoxy-4-methylphenyl) propane (DOM), r-(-)-2-amino-1-(2,5-dimethoxy-4-methylphenyl) butane (BL-3912A) and 5-hydroxytryptamine on non-innervated vascular smooth muscle.

Isolated strips of sheep umbilical arteries contracted in the presence of R-(-)-2-amino-1-(2,5-dimethoxy-4-methylphenyl) butane (BL3912A). These contractions faded over an hour period and at this time BL3912A antagonized contractions to R-(-)-DOM, 5-hydroxytryptamine (5-HT) but not to angiotensin. The initial contraction produced by BL3912A was antagonized by cinanserin, a 5-HT antagonist. These experiments indicate that BL3912A can be classified as a partial agonist of 5-HT receptors in sheep umbilical arteries.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗