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At least 19 recordsLinked to original sources
PubMed1978

3-Tertiary amino-1-aryloxy- or aryl-propanes and -propan-2-ols and some related compounds.

The synthesis and pharmacological activity of some 3-tertiary amino-1-aryloxy- or 1-aryl-, 1-thiophenoxy and 1-anilino-propan-2-ols and -propanes, particularly those derived from N-phenylpiperazines are described. Effect of substituents (nature/position) on the phenyl ring, the phenoxy ring as well as alteration in the hydroxylic function vis-à-vis the structure-activity relationships (SAR) are discussed. In general, the 1-aryloxy compounds have hypotensive activity--this being more pronounced in those carrying an o-substituent on the phenyl ring, while m and p-substituted derivatives have their effect primarily on the CNS. Variations in the phenoxy moiety do not significantly alter the intrinsic activity. The 1-aryl compounds, on the other hand, have significant CNS activity, which is markedly affected by the substituents on the 1-aryl residue.

1-Propanol↗
PubMed1978

beta-Adrenergic blocking agents. 18. 1-(Aryloxy)-3-(arylthioalkylamino)propan-2-ols and 1-substituted alkylthioamino-3-(aryloxy)propan-2-ols.

The synthesis is described of a seris of derivaties of 1-(aryloxy)-3-(arylthioalkylamiho)propan-2-ols and 1-(alkylthioamino)- and 1-(aralkylamino)-3-(aryloxy)propan-2-ols. These compounds were investigated for their beta-adrenoreceptor blocking properties and their selectivity of action for the cardiac beta1 receptor. The structure-activity relationships are discussed with particular reference to the effects of the sulfur, sulfoxide, and sulfone groups on beta-adrenoreceptor blocking potency and selectivity.

Adrenergic beta-Antagonists↗
PubMed1991

Oxidative denitrification of 2-nitropropane and propane-2-nitronate by mouse liver microsomes: lack of correlation with hepatocytotoxic potential.

2-Nitropropane (2-NP) is an industrial chemical with hepatotoxic and genotoxic properties. It exists in chemical equilibrium with propane-2-nitronate, which is much more genotoxic than 2-NP. In this work the link between toxicity and metabolism of 2-NP and its nitronate was investigated. To that end 2-NP or propane-2-nitronate were incubated with murine hepatic microsomes at concentrations of up to 10 mM, and generation of nitrite was measured as product of metabolic oxidation of the two species. Under the acidic reaction conditions of the colorimetric nitrite assay propane-2-nitronate decomposed chemically to nitrite. Therefore an ion-pair HPLC assay at neutral pH was developed which enabled determination of nitrite formed from the nitronate. The rate of metabolic nitrite generation from propane-2-nitronate was 5-10-fold that obtained with 2-NP. Metabolism of either species to nitrite was dependent on the presence in the incubate of viable microsomes and of NADPH, and it was inhibited in the presence of carbon monoxide or the cytochrome P-450 inhibitor SKF525A. Acetone could also be measured as a metabolite of 2-NP. Optical difference spectra were recorded in mixtures of propane-2-nitronate with liver microsomes from phenobarbital-pretreated rats. The spectral dissociation constant was found to be 30 mM, which compares with 10 mM reported for 2-NP. 2-NP and propane 2-nitronate were incubated with mouse hepatocytes in suspension and cytotoxicity was determined by measurement of leakage of cellular lactate dehydrogenase into the medium. Both species were hardly toxic, as concentrations of 20 mM were required to elicit significant damage to the cells. The results demonstrate that propane-2-nitronate, like 2-NP, undergoes microsomal oxidative denitrification, probably catalysed by cytochrome P-450. Metabolism of both species occurs at markedly different rates, but the difference in metabolism is not reflected by a difference in hepatocytotoxic potential.

Animals↗
PubMed1990

Propane-1,2-diol as a potential component of a vitrification solution for corneas.

Any method of cryopreservation of the cornea must maintain integrity of the corneal endothelium, a monolayer of cells on the inner surface of the cornea that controls corneal hydration and keeps the cornea thin and transparent. During freezing, the formation of ice damages the endothelium, and vitrification has been suggested as a means of achieving ice-free cryopreservation of the cornea. To achieve vitrification at practicable cooling rates, tissues must be equilibrated with high concentrations of cryoprotectants. In this study, the effects of propane-1,2-diol on the structure and function of rabbit corneal endothelium were studied. Corneas were exposed to concentrations of propane-1,2-diol ranging from 10 to 30% v/v in a Hepes-buffered Ringer's solution containing glutathione, adenosine, 5 mmol/liter sodium bicarbonate, and 6% w/v bovine serum albumin. Endothelial function was assessed by monitoring corneal thickness during perfusion of the endothelial surface at 34 degrees C for 6 hr. Exposure to 10-15% v/v propane-1,2-diol was well tolerated for 20 min at 4 degrees C when the cryoprotectant was removed in steps or by sucrose dilution. However, exposure to 25% v/v propane-1,2-diol for 20 min at 0 or -5 degrees C was consistently tolerated only when 2.5% w/v chondroitin sulfate was included in the vehicle solution. Exposure to 30% v/v propane-1,2-diol was harmful at -5 and -10 degrees C. The endothelial damage following exposure to 30% v/v propane-1,2-diol was probably the result of a toxic effect rather than osmotic stress. Although 25% v/v propane-1,2-diol does not vitrify at cooling rates that are practicable for corneas, it could at this concentration form a major component of a vitrification solution comprising a mixture of cryoprotectants.

Animals↗
PubMed1991

Investigation of the chemical basis of nitroalkane toxicity: tautomerism and decomposition of propane 1- and 2-nitronate under physiological conditions.

Unlike primary nitroalkanes, such as 1-nitropropane, the secondary nitroalkane 2-nitropropane is geno- and hepatotoxic. Nitroalkanes exist in equilibrium with alkane nitronates. In order to investigate the relationship between nitroalkane toxicity and generation and stability of nitronates, propane 1- or 2-nitronate (4-6 mM) were incubated in buffer (pH 3.8 -7.4) in the absence or presence of cysteine. Equilibrium formation and degradation were studied by 1H-NMR spectroscopy and ion pair HPLC chromatography. Propane 1-nitronate generated 1-nitropropane rapidly and almost quantitatively. In the case of propane 2-nitronate equilibrium at pH 7.4 was reached within 8 h, when 48% of initial nitronate had tautomerised to 2-nitropropane. The pKa of the reaction 2-nitropropane less than--greater than propane 2-nitronate measured by HPLC was 7.63. Equilibrium formation, hydrolysis and reduction of nitronates were pH-dependent and, in the case of propane 2-nitronate, yielded mainly acetone, nitrite and acetone oxime, apart from 2-nitropropane. Hydrolysis of propane 2-nitronate (4 mM) to nitrite was modulated by cysteine (4 mM) and p-methoxyphenol (0.4 mM). At pH 7.4 they increased nitrite generation by 300 and 28%, respectively, at pH 4.8 they decreased nitrite formation by 91 and 82%, respectively, probably by scavenging radical intermediates. Differences between nitroalkanes in terms of content of nitronate tautomer at equilibrium are probably an important chemical determinant of their toxic potential.

Animals↗
PubMedDate not supplied

Effect of bromine and chlorine positioning in the induction of renal and testicular toxicity by halogenated propanes.

A series of halogenated propanes were studied for renal and testicular necrogenic effects in the rat and correlated to their ability to induce in vivo renal and testicular DNA damage and in vitro testicular DNA damage. 1,2-Dibromo-3-chloropropane (DBCP) and 1,2,3-tribromopropane were most potent in causing organ damage in both kidney and testes. Extensive necrosis was evident at 85 mumol/kg in kidney and at 170 mumol/kg in testis. The dibromomonochlorinated analogue 1,3-dibromo-2-chloropropane was less organ toxic than DBCP and 1,2,3-tribromopropane, but induced more organ damage than the dichloromonobrominated analogues 1-bromo-2,3-dichloropropane and 1,3-dichloro-2-bromopropane. Dihalogenated propanes were even less necrogenic. These observed differences in toxic potency between the halogenated propanes could not be explained by relative differences in tissue concentrations. The ability of the halogenated propanes to induce DNA damage in vivo correlated well with their ability to induce organ damage. However, DNA damage occurred at lower doses and at a shorter period of exposure than organ necrosis. This indicates that DNA damage might be an initial event in the development of organ necrosis by halogenated propanes in general. Further, testicular DNA damage induced by the halogenated propanes in vivo correlated well with the DNA damage observed in isolated testicular cells in vitro, showing that toxicity was due to in situ activation. The numbers, positions, and the types of halogen substituents appear to be important determinants in causing DNA damage and necrogenic effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

The effects of an antimetastatic agent, (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane (ICRF 159), on platelet behavior.

Some agents that inhibit platelet aggregation, e.g., aspirin and dipyridamole, ahve been reported to prevent metastasis formation. To see whether inhibition of platelet aggregation could account for the antimetastatic action of (plus or minus)-1,2- bis(3,5-dioxopiperazin-1-yl)propane, this compound was investigated in vivo for any effects on platelet behavior and thrombogenesis. (plus or minus)-1,2-Bis(3,5-dioxopiperazin-1-yl)propane inhibited the formation of platelet thrombi in blood vessels on the surface of the rat brain and in the hamster cheek pouch. 1,2-Bis(dioxo-4-methylpiperazin-1-yl)ethane, a closely related analog of (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane, but without antimetastatic action, inhibited thrombus formation in vivo as effectively as (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane. It seems unlikely therefore that the antimetastatic action of (plus or minus)-1,2-bis(3,5-dioxopiperazine-l-yl)propane derives from its effects on thrombogenesis. Neither platelet numbers nor the ionized plasma calcium concentrations were changed after (plus or minus)-1,2-bis(3,5-dioxopiperazin-l-yl)propane administration.

Animals↗
PubMed1991

Corneal tolerance of vitrifiable concentrations of propane-1,2-diol.

The merit of corneal cryopreservation by vitrification as opposed to conventional freezing is the avoidance of ice damage which is believed to disrupt the integrity of the corneal endothelium resulting in loss of corneal transparency. The cornea must be equilibrated with high concentrations of cryoprotectant in order to achieve vitrification at practicable cooling rates. In an earlier study, corneas were exposed to 3.4 mol/liter propane-1,2-diol (Rich and Armitage (1990) Cryobiology 27, 42-54). The present study exposed rabbit corneas to concentrations of propane-1,2-diol between 3.4 and 5.4 mol/liter in a Hepes-buffered Ringer's solution containing glutathione, adenosine, 5 mmol/liter sodium bicarbonate, 6% (w/v) bovine serum albumin, and 2.5% (w/v) dextran sulfate. Dextran sulfate was as effective as chondroitin sulfate at improving endothelial tolerance of 3.4 mol/liter propane-1,2-diol. This beneficial effect may be linked to the polyanionic nature of these molecules. Corneas exposed to 5.4 mol/liter propane-1,2-diol were cooled in liquid nitrogen vapor at a temperature of -140 degrees C for 2 h. Warming was achieved by direct transfer to a dilution solution at -10 degrees C. Endothelial function was assessed by monitoring corneal thickness during perfusion of the endothelial surface at 34 degrees C for 6 h. Endothelial structure was observed by specular microscopy during the perfusion and by scanning electron microscopy after perfusion. Corneas tolerated exposure to 3.4 mol/liter propane-1,2-diol for 20 min at 0 degrees C and to 4.1 mol/liter for 10 min at -10 degrees C. Exposure to 4.8 and 5.4 mol/liter for 10 min at -10 degrees C caused endothelial damage, although a degree of endothelial function was retained. Function following exposure to 5.4 mol/liter was improved by reducing the temperature of exposure to -15 degrees C. Corneas cooled after exposure to 5.4 mol/liter propane-1,2-diol for 10 min at -15 degrees C apparently vitrified, but devitrified on warming. The corneas swelled to such an extent during perfusion that the endothelium could not be viewed by specular microscopy, subsequent scanning electron microscopy showed a severely disrupted endothelium.

Animals↗
PubMedDate not supplied

The carcinogenic response in mice to the topical application of propane sultone to the skin.

The carcinogenic effects of limited and repeated skin applications of propane sultone were investigated in three strains of mice, CF1, C3H and CBah (a hairless strain). Propane sultone was shown to be carcinogenic when given as a single application of a 25% w/v solution in toluene and also following twice weekly application of a 2.5% w/v solution for up to 58 weeks. More limited exposure to 2.5% w/v solutions of propane sultone resulted in a few skin tumours, although the incidences were not statistically significant. Most neoplasms were papillomas or carcinomas, although a small number of mesenchymal tumours of dermal origin also developed. No skin neoplasms were found in any control mice. The skin application of propane sultone was associated with a statistically significant increase in the incidence of systematic neoplasia in CFl and C3H mice. The exposed CFl mice had a higher incidence of neoplasms of lymphoreticular and lung origin, while female C3H mice showed a higher incidence of mammary gland and uterine tumours. In mice exposed to beta-propiolactone as a positive control, neoplasms developed at the site of application but, there was no evidence of increased systemic neoplasis in contrast to the findings with ptopane sultone.

Animals↗
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↗
PubMed1989

Effect of propan-2-ol on enzymic and structural properties of elongation factor G.

Elongation factor G (EF-G) can support a GTPase activity in vitro even in the absence of ribosomes when propan-2-ol is present [GTPasep; De Vendittis, Masullo & Bocchini (1986) J. Biol. Chem. 261, 4445-4450]. In the present work the GTPasep activity of EF-G was further studied by investigating (i) the effect of ionic environment on GTPasep and (ii) the influence of propan-2-ol on the molecular structure of EF-G as determined by fluorescence and c.d. measurements. In the presence of 1-300 mM univalent cations (M+) alone, no detectable GTPasep activity was measured; however, in the presence of 1 mM-Mg2+ a considerable stimulation was observed at 40 mM-Li+ or 75 mM-NH4+. Among bivalent cations (M2+), 1 mM-Sr2+, 2-5 mM-Ca2+ and 1 mM-Ba2+ were the most effective, but, in the presence of 75 mM-NH4+, Mg2+ and Mn2+ became the most efficient, whereas the stimulation by other M2+ species was considerably decreased. C.d. measurements showed that the alcohol increased the mean molar residue ellipticity of EF-G at 285 nm, but not at 220 nm. As estimated from fluorescence measurements, in the presence of 20% (v/v) propan-2-ol the value of the dissociation constant of the complex formed between EF-G and 8-anilino-1-naphthalene-sulphonate decreased from 8 to 5 microM; similarly, the number of binding sites on EF-G for the fluorescent probe decreased from 13 to 6. Finally, the alcohol enhanced the quenching of the intrinsic fluorescence of EF-G caused by either acrylamide or KI. The data support the hypothesis that propan-2-ol induces moderate conformational changes of EF-G that make the catalytic centre accessible to the substrate even in the absence of ribosomes. Kinetics of GTPasep studied at different temperatures did not reveal additional structural changes of EF-G occurring with time or temperature.

1-Propanol↗
PubMedDate not supplied

The protection against and treatment of a liquid propane freeze injury: an experimental model.

Liquid propane causes a severe, deep thermal injury in unprotected tissue. Delayed surgical intervention, as for thermal burns, has been the gold standard of treatment. An animal model of liquid-propane injury was devised to document injury, to demonstrate a better method of protection, and to define an appropriate management protocol. Twenty-eight rats were classified into four groups: unprotected tissue (n = 8), skin covered with wool (n = 8), skin covered with Neoprene (Wm. H. Horn & Brothers Inc., Philadelphia, Pa.) (n = 8), and skin covered with wool plus Neoprene (n = 4). Each group was subdivided into two exposure times: 6 seconds and 30 seconds. The mean temperatures +/- standard error of the mean of the various tissue levels initially and at 6 and 30 seconds of exposure were determined. Histologic examination demonstrated that full-thickness tissue necrosis occurred in unprotected and wool-covered tissue. Areas that were covered with Neoprene showed intact skin and subcutaneous tissue with underlying muscle necrosis. Examination of the tissue that was covered with wool plus Neoprene showed no histologic damage. There was no sign of tissue regeneration at the wound periphery, and there was no histologic difference in any group, whether the examination took place at 1 or 5 days after injury. This study demonstrated that the best form of protection appears to be a wool glove liner covered with a Neoprene glove. The histologic evidence suggests that a liquid-propane injury to unprotected tissue should be managed aggressively with early excision and grafting.

Animals↗
PubMed1992

Warehouse workers' headache. Carbon monoxide poisoning from propane-fueled forklifts.

We reviewed over 220 cases of acute carbon monoxide (CO) poisoning and now report on 17 patients whose poisoning occurred from the indoor use of propane-fueled forklifts. All patients in this series presented with neurologic symptoms or persistent headache and were given hyperbaric oxygen to resolve their symptomatology. We investigated the concentration of CO in the exhaust emissions of 12 propane-fueled forklifts used in various workplaces in our location. The average CO concentration in the exhaust during engine idling was 36,000 parts per million (3.6%). This value decreased slightly to 30,000 ppm (3.0%) at working engine speed. Measurements of exhaust flow indicate CO production rates of approximately 60 liters per minute at working engine speed. These quantities of CO constitute a significant occupational exposure risk to workers using propane-fueled forklifts in unventilated indoor environments.

Acute Disease↗
PubMed1991

Study of polymeric systems based on 2,2 bis-4(2-hydroxy-3-methacryloyl-oxypropoxy) phenyl propane.

2,2 bis-4(2-hydroxy-3-methacryloyloxypropoxy) phenyl propane is the basic monomer for a large number of proprietary dental composite filling materials. In this paper, studies have been made of its copolymers with various comonomers. 2,2 bis-4(2-hydroxy-3-methacryloyloxypropoxy) phenyl propane--tetrahydrofurfuryl methacrylate copolymers, at about the 95/5% v/v level, showed an enhanced modulus over that of the test material itself, to give a Young's modulus of -4.8 GPa. This reflected an enhanced activation energy of the glass transition temperature, indicating a very specific free volume effect of the diluent monomer. Further studies 2,2 bis-4(2-hydroxy-3-methacryloyloxypropoxy) phenyl propane-tetrahydrofurfuryl methacrylate room temperature polymerized copolymers showed that enhanced modulus could be achieved by including in the system small amounts of inhibitor; 0.3% v/v 2,6 di-tertiary butyl phenol elevated the Young's modulus of a benzoyl peroxide--NN-dihydroxy ethyl p-toluidine cured system from 3.1 to 3.6 GPa. Such resins may be useful in improved dental fissure sealants and composite filling materials.

Benzoyl Peroxide↗
PubMed1991

The effect of propane-diols on the intestinal uptake of nutrients and brush border membrane enzymes in the rat.

The effect on rats of oral doses (38.66 mM/kg body wt) of propane-1,2-diol (PD) administered daily for 10 (Group 1), 20 (Group 2), and 30 days (Group 3) was investigated. Weight gain was initially retarded (P less than 0.05) in Group 1, but was later reversed and elevated significantly (P less than 0.05) in Groups 2 and 3 as compared with their respective controls receiving an equal volume of saline. PD showed a tendency toward enhancing the activities of various enzymes involved in terminal digestion, with the significant effect exerted in few groups on sucrase (P less than 0.05), lactase (P less than 0.05), and gamma-glutamyl transpeptidase (P less than 0.05) when compared with the respective controls. Absorption of D-glucose, glycine, L-aspartic acid, L-lysine, and calcium was elevated and was especially significant in Groups 2 and 3 (P less than 0.001). The structural integrity of the jejunal surface was retained for the most part. A similar examination of the effects of PD was also carried out in vitro to ascertain whether PD itself or its metabolites are involved in its action. The in vitro effects of propane-1,2-diol were compared with those of the more toxic compound propane-1,3-diol. The former exerted greater inhibitory action on the activities of the disaccharidases. The degree of inhibition was in the order sucrase much greater than lactase greater than maltase. The kinetic data revealed that inhibition by 1,2-diol in native and detergent solubilized sucrase is noncompetitive, with Ki values in the range of 0.35-0.41 M. The two diols did not alter the nutrient transport in the brush border membrane vesicles. The present work on rats indicates that PD may influence the intestinal digestive and absorptive functions in vivo and that this in vivo effect of PD is different from that observed in vitro suggesting that the nutritional and toxicological effect of PD may be mediated by different mechanisms.

Administration, Oral↗
PubMed1979

Cardioselectivity of beta-adrenoceptor blocking agents 1. 1-[(4-Hydroxyphenethyl)amino]-3-(aryloxy)propan-2-ols.

A series of 1-[(4-hydroxyphenethyl)amino]-3-(aryloxy)propan-2-ols was synthesized together with several 1-[(3,4-dimethoxyphenethyl)amino]-3-(aryloxy)propan-2-ols. Their affinity to beta 1- and beta-2-adrenoceptors was determined and compared with the affinity of known beta-blockers. We were able to confirm the substantial cardioselectivity of 1-(3,4-dimethoxyphenethyl)-3-[(4-substituted aryl)oxy]propan-2-ols when compared to those with a 1-(4-hydroxyphenethyl) group. An increase in the size of the 4 substitutent of the 3-(aryloxy) moiety to caproamido leads to a substantially higher affinity for the beta 1--adrenoceptor of rat ventricular muscle in the presence of the 3,4-dimethoxyphenethyl than in the presence of the 4-hydroxyphenethyl or isopropyl group; this combination also gave the highest cardioselectivity.

Adrenergic beta-Antagonists↗
PubMed1975

Effect of a single oral dose of methanol, ethanol and propan-2-ol on the hepatic microsomal metabolism of foreign compounds in the rat.

Methanol and ethanol administered to rats as a single oral dose increased aniline hydroxylation by the hepatic microsomal fraction by a maximum of 169 and 66% respectively, whereas aminopyrine demethylation was inhibited by 51 and 61%. The concentration of microsomal cytochrome P-450, and the activities of NADPH-cytochrome c reductase and NADPH-cytochrome P-450 reductase were unchanged. Propan-2-ol, administered as a single oral dose, increased microsomal aniline hydroxylation by 165% and increased aminopyrine demethylation by 83%. The concentration of cytochrome P-450 was unchanged whereas NADPH-cytochrome c reductase and NADPH-cytochrome P-450 reductase were both increased by 38%. Methanol, ethanol and propan-2-ol administration resulted in a decreased type I spectral change but had no effect on the reverse type I spectral change. Methanol administration decreased the type II spectral change whereas ethanol and propan-2-ol had no effect. Cycloheximide blocked the increases in aniline hydroxylation and aminopyrine demethylation but could not completely prevent the decreases in aminopyrine demethylation. The increases in aniline hydroxylation were due to an increase in V, but Km was unchanged. The ability of acetone to enhance and compound SKF 525A to inhibit microsomal aniline hydroxylation was decreased by the administration of all three alcohols. The decrease in the metabolism of aminopyrine may result from a decrease in the binding to the type I site with a consequent failure of aminopyrine to stimulate the reduction of cytochrome P-450. Methanol administration may lead to an increase in aniline hydroxylation because of a failure of aniline to inhibit cytochrome P-450 reduction.

1-Propanol↗