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At least 775 records · Page 43Linked to original sources
PubMed1979

Release from the Crabtree effect by hypoxic cell radiosensitizers.

The Crabtree effect can be observed when the O2 consumption of tumour cells or of mammalian cells grown in culture is measured in physiological medium containing glucose. The effect of 2 hypoxic cell radiosensitizers, misonidazole and NDPP, on the O2 consumption of Ehrlich ascites tumour cells was compared in media with and without glucose. A stimulatory effect on O2 consumption was found for 5--20mM misonidazole as well as for 0.5mM NDPP, both in media containing 10(-2)M glucose. Thus glucose induced a Crabtree effect in Ehrlich tumour cells, expressed as 38--45% inhibition of O2 consumption relative to that in the same medium without glucose. The stimulatory effect of misonidazole and NDPP on O2 utilization in medium with glucose undoubtedly appeared as a release from the Crabtree effect.

Animals↗
PubMed1984

Propafenone disposition kinetics in cardiac arrhythmia.

Propafenone disposition kinetics were studied after intravenous and oral doses in patients with ventricular arrhythmias. Plasma concentration-time data were fit to a two-compartment model for all but one patient, whose data required fitting to a three-compartment model. The model-independent calculated values of clearance, steady-state volume of distribution, and terminal t1/2 were 11.2 +/- 4.8 ml/min/kg, 3.6 +/- 2.1 l/kg, and 5.0 +/- 3.6 hr. After 5 days on oral propafenone, elimination t1/2 was 6.2 +/- 3.3 hr. The longer t1/2s and the estimates of steady-state bioavailability above 100% suggests that clearance decreases during chronic oral dosing. Considerable intersubject variability was noted in all disposition parameters.

Adult↗
PubMed1984

Bupropion does not antagonize cardiovascular actions of clonidine in normal subjects and spontaneously hypertensive rats.

Tricyclic antidepressants (TADs) are known to antagonize the hypotensive and sedative actions of clonidine. We compared the effects of bupropion and imipramine pretreatment on the acute hypotensive and sedative actions of clonidine in eight normotensive male subjects in a randomized, double-blind crossover study. Pretreatment with bupropion, 100 mg by mouth three times a day for 9 days, had no effect on baseline supine blood pressure (BP) and heart rate (HR) and did not modify the hypotensive, bradycardic, and sedative actions of clonidine. Imipramine, 25 mg by mouth three times a day for 9 days, increased supine and standing HR and decreased standing systolic BP. In half the subjects the hypotensive action of clonidine was reduced 40% to 50% by imipramine. The specific binding of 3H-yohimbine to alpha 2-receptors of platelet membranes was not affected by pretreatment with either antidepressant. In spontaneously hypertensive rats, 16 days of bupropion, 25 mg/kg subcutaneously, had no effect on baseline BP and HR and did not antagonize the hypotensive and bradycardic effects of clonidine, 5 mg/kg iv. Pretreatment with desipramine, 5 mg/kg subcutaneously for 16 days, accelerated baseline HR and reduced cardiovascular actions of clonidine. These observations suggest that not all antidepressants antagonize the effects of clonidine. If the negative interaction between TADs and clonidine is a result of sensitivity of alpha 2-receptors, these receptor changes are not the common denominator of antidepressant activity and may only be seen with TADs.

Adult↗
PubMed1985

Pharmacokinetics of bupropion and its major basic metabolites in normal subjects after a single dose.

The pharmacokinetics of bupropion (BUP) and its three major basic metabolites (the erythroamino alcohol [EB], the threoamino alcohol [TB], and the hydroxy [HB] metabolites) were characterized after a single, oral, 200 mg dose of BUP in six healthy men. Twenty-one sequential plasma samples for analysis by HPLC were drawn from each subject over the 56-hour period after dosing. Pharmacokinetic analyses were by noncompartmental methods. The mean elimination t1/2 values of BUP, TB, EB, and HB were 9.8, 19.8, 26.8, and 22.2 hours, respectively. The mean plasma AUCs of TB and HB were 2.4 and 10.3 times greater, respectively, than that for BUP. Because of the substantial presence of these metabolites in systemic circulation, further studies are recommended to understand further their roles in the clinical profile of this new antidepressant.

Adult↗
PubMed1985

Metabolite cumulation during chronic propafenone dosing in arrhythmia.

The cumulation of propafenone and two of its metabolites, 5-hydroxypropafenone (5-OHP) and N-depropylpropafenone (NDPP), was examined in patients with frequent ventricular ectopy. After 2 weeks of propafenone therapy (300 mg twice a day), propafenone was discontinued and blood samples were drawn for 24 hours. The mean (+/- SD) steady-state concentrations of propafenone, 5-OHP, and NDPP were 1010 +/- 411, 174 +/- 113, and 179 +/- 93 ng/ml. The concentration ratios of 5-OHP/propafenone and NDPP/propafenone were 0.177 +/- 0.049 and 0.227 +/- 0.203. Plasma concentrations of 5-OHP and NDPP did not decay in a log-linear manner during the sampling period and thus estimates of their disappearance t1/2s were not possible. At 24 hours after propafenone dosing, concentrations of 5-OHP and NDPP were 63% +/- 37% and 50% +/- 21% of their mean steady-state levels. Our data indicate that these propafenone metabolites cumulate in the plasma during chronic oral propafenone therapy, and that their clinical role needs to be elucidated.

Adult↗
PubMed2006

Interactions between different solar UVB/UVA filters contained in commercial suncreams and consequent loss of UV protection.

A systematic investigation of two well-known and popular commercial suncreams reveals significant degradation when exposed to simulated UV sunlight at an irradiance corresponding to natural sunlight. We have examined the photochemistry of two widely used sunscreen active agents in pure solvents separately and together (in solution), and in neat form, as well as their photochemistry when present in the actual suncream emulsion (as thin films on a glass substrate) since their combination typically produces suncreams with high sun protection factors (SPF): (1a) octyl methoxycinnamate (OMC; octinoxate) and (2a) 4-tert-butyl-4'-methoxydibenzoylmethane (also known as avobenzone and Parsol 1789), present in the two suncream formulations in combination with others (one also contained TiO2). Intermediates and/or photoproducts were identified by UV/visible spectroscopy, HPLC and liquid chromatographic/mass spectral methods, and by both 1H and 13C-NMR techniques. Structural assignments of the substrates produced were aided by examining model systems {viz. ethyl cinnamate (1b) and dibenzoylmethane (2b)} of the two sunscreen active agents. Irradiation of the cinnamates and the diketones together led to a [2 + 2] photocycloaddition process yielding cinnamate dimers and cyclobutylketone photoadducts that subsequently fragmented into substituted oxopentanoates and oxobutanoates. Similar findings were observed when the two active agents were simultaneously present in the same suncream emulsion.

Chalcones↗
PubMed1972

The peroxidase-catalysed oxidation of a chalcone and its possible physiological significance.

1. Crystalline horseradish peroxidase catalysed the oxidation of 2',4,4'-trihydroxychalcone (isoliquiritigenin) in the presence of trace amounts of hydrogen peroxide under aerobic conditions. One atom of oxygen was consumed for each molecule of substrate. 2. The reaction course comprised a lag phase and a linear phase. The optimum pH for the linear phase of the reaction was about 7.5. The length of the lag phase decreased with increasing pH. It is suggested that the chalcone anion is the actual substrate for the reaction. 3. No evidence for the production of reducing free radicals or perhydroxyl radicals during the reaction could be found. 4. 4',7-Dihydroxyflavonol and 4',6-dihydroxyaurone were isolated from the reaction mixture. The immediate products of the reaction may have included 3,4',7-trihydroxyflavanone and 4',6-dihydroxy-2-(alpha-hydroxybenzyl)coumaran-one, which can be readily converted non-enzymically into the flavonol and aurone respectively. 5. A similar reaction was catalysed by cell-free extracts of hypocotyls of Phaseolus vulgaris. 6. The physiological significance of the reaction is discussed in terms of a possible free-radical mechanism. An analogy may exist between flavonoid biosynthesis and lignin formation.

Aerobiosis↗
PubMed2003

Methcathinone is a substrate for the serotonin uptake transporter.

We previously reported that the psychostimulant drug methcathinone inhibits serotonin accumulation via the plasma membrane serotonin uptake transporter. By analogy to known substrates for the serotonin transporter, we hypothesized that methcathinone is also a substrate for this transporter and that inhibition of serotonin uptake by methcathinone occurs in part through competition for substrate recognition sites within the transporter. To test the hypothesis we preloaded human platelets with [3H]5-HT then superfused the platelets with either methcathinone or with the known serotonin uptake transporter substrate para-methylthioamphetamine. Under superfusion conditions, transporter substrates will evoke an increase in released [3H]5-HT through a carrier-mediated exchange process. For direct assessment of methcathinone transport via the serotonin uptake transporter, we tested whether [3H]methcathinone would be accumulated by cells stably expressing the cloned human serotonin uptake transporter (293SERT cells). Supporting the hypothesis, superfusion of [3H]5-HT-containing platelets with methcathinone or with para-methylthioamphetamine produced a large increase in tritium efflux. The efflux declined when the drugs were removed. When increasing concentrations of [3H]methcathinone were incubated with 293SERT cells under conditions used to assess serotonin transport, saturable, single-site accumulation of radiolabel was observed. The uptake of [3H]methcathinone was temperature, inhibitor, and sodium-sensitive, and was not observed in wild-type HEK 293 cells. Non-linear regression analysis of specific [3H]methcathinone uptake produced values for KM and Vmax of 244+/-51 nM and 202+/-25 fmol/min./mg protein, respectively. These data support the notion that the reported serotonergic neurotoxicity of methcathinone may arise through accumulation of the drug within serotonergic neurones.

Blood Platelets↗
PubMed1976

[Propafenon, a new anti-arrhythmic drug (author's transl)].

Propafenon, at an initial oral dose of 900 mg, proved an effective anti-arrhythmic drug in 34 patients with frequent ventricular and(or) supraventricular extrasystoles at rest. Long-term ECG monitoring of seven patients revealed that this effect lasted about eight hours. It can be maintained by an oral dose of 300 mg propafenon at eight-hourly intervals, as demonstrated in 21 further patients. Rapid anti-arrhythmic action was achieved in six acute cases with 1.0-1.5 mg propafenon per kg body weight by quick infusion, and lasted for one to one-and-a-half hours. In such cases the drug should, therefore, be given synchronously by the oral route. Side effects related to the gastrointestinal tract, sinus automatism as well as atrio-ventricular and intraventricular conduction, but in no case were very serious.

Administration, Oral↗
PubMed1978

[Propafenon and lidoflazine in chronic atrial fibrillation and flutter (author's transl)].

60 patients with chronic atrial fibrillation and flutter were randomly allotted to two groups and treated alternately with two different therapy regimes. 30 patients (group I) received lidoflazine in increasing dosage up to 480 mg/24 h and in cases where there was no conversion to sinus rhythm propafenon in a maximal daily dosage of 1800 mg orally. The duration of treatment was limited to 4 days for each substance. 30 patients (group II) were treated in the reverse order, i.e. propafenon and in cases of ineffectiveness with lidoflazine. Atrial fibrillation could be overcome in 21 patients in group I and in 23 patients in group II. The combined success rate in both groups was 73%. The conversion rates for the individual substances were 41% for propafenon (17 out of 41 patients) and 59% for lidoflazine (27 out of 46 patients). The difference was not statistically significant. Successive use of both substances leads to an increased conversion rate. Dangers arising from therapy are a conduction inhibitory action and depression of sinus node function as far as propafenol is concerned and the risk of ventricular ectopy and tachyarrhythmia in lidoflazine.

Aged↗