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The metabolic disposition of [14C]pivhydrazine, [14C]mebanazine, and [14C]benzylhydrazine in the rat.

The hydrazine drugs, [14C]pivhydrazine and [14C]mebanazine and the related compound [14C]benzylhydrazine were readily absorbed from the rat gut and the radioactivity was excreted mainly in urine. The major urinary metabolite of pivhydrazine and benzylhydrazine was [14C]hippuric acid, whereas mebanazine was shown to be excreted largely unchanged. Biliary excretion (21 and 24%, respectively) of radioactive material was observed after administration of [14C]pivhydrazine and [14C]mebanazine to bile duct-cannulated rats but only small amounts (approximately 3%) were excreted in bile after [14C]benzylhydrazine administration. The major biliary metabolites of pivhydrazine and mebanazine are acid-labile conjugates, possibly N-glucuronides. In vitro studies with rat liver homogenate suggest that benzylhyrazine may be an intermediate in the metabolism of pivhydrazine. The distribution of radioactivity in the rat 7 days after the administration of [14C]pivhydrazine and [14C]pivhydrazine and [14C]mebanazine is described.

Animals↗
PubMed1975

Induction and suppression of hepatic and extrahepatic microsomal foreign-compound-metabolizing enzyme systems by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on a number of hepatic and extrahepatic foreign-compound-metabolizing enzyme systems in microsomes from rats, rabbits and guinea pigs were investigated. Following TCDD treatment, the N-demethylation of benzphetamine, aminopyrine and ethylmorphine was suppressed in hepatic microsomes from male but not from female rats. However, both cytochrome P-450 and benzpyrene hydroxylase were significantly stimulated in hepatic microsomes from both male and female rats at doses as small as 1 mug TCDD/kg body weight. The inductive effect on rat hepatic microsomal enzymes was considerably more persistent than the suppressive effect. Following a single oral dose of 25 mug TCDD/kg weight, benzpyrene hydroxylase of male rat liver microsomes remained significantly elevated for 73 days but the suppression of benzphetamine N-demethylase had gone after 35 days. The induction of benzpyrene hydroxylase in male rat liver microsomes by TCDD was independent of the age of the rat and the levels to which this enzyme was increased was similar in male rats of all ages. However, the suppression of benzphetamine N-demethylase in male rat liver microsomes was age related: the suppression was seen only in adult animals and in the very young (10 days old) the enzyme was actually induced by TCDD. Inductive effects appeared in both smooth and rough-surfaced hepatic microsomes from male rats but the suppression of N-demethylation occurred only in the smooth-surfaced microsomes (SER). In microsomes from extrahepatic tissues of the rat, induction of mixed-function oxidases (MFOs) by TCDD occurred only in the kidney. However, UDPglucuronyltransferase was induced in microsomes from lung, kidney, intestine and brain but not testes. The response in the rabbit and guinea pig to TCDD differed considerably from that in the rat. Benzpyrene hydroxylase was unaffected in hepatic microsomes from the guinea pig and actually suppressed in microsomes from rabbit liver. Benzphetamine N-demethylase was also suppressed in rabbit liver microsomes. Glucuronyl-transferase was unaffected by TCDD in microsomes from liver, lung or kidney of the rabbit and guinea pig. The only lung enzyme responsive to TCDD was biphenyl 4-hydroxylase of the rabbit and guinea pig. Suppression was not observed in any of the extraheptic tissues studied and may be confined to only certain hepatic systems.

Animals↗
PubMed1978

Gas phase carboxylate anions fron p-nitrobenzyl esters of fatty acids.

Gas phase carboxylate anions have been efficiently generated from the p-nitrobenzyl esters of nine fatty acids ranging in size from C6 to C22. The process involves the dissociative resonance capture of 2.9 e V electrons by the derivatives. The procedure is specific and gives the carboxylate anions as the base peak in all but two of the derivative. The technique gives extremely simple spectra, with little additional fragmentation and no rearrangement ions.

Benzyl Compounds↗
PubMed1979

Quantitative analysis of tiamenidine in human plasma by gas chromatography mass spectrometry of a dibenzyl derivative.

A gas chromatography mass spectrometry method has been developed and evaluated for the quantitative analysis of tiamenidine in plasma. Tiamenidine and internal standard are extracted from basified plasma, converted to dibenzyl derivatives by reaction with benzyl bromide and potassium t-butoxide in the presence of 18-crown-6 ether prior to analysis by selected ion monitoring. The method can be used over the range 0.2--10 ng ml-1 with a coefficient of variation of better than 20% at 1 ng ml-1.

Alkylation↗
PubMed1975

Pharmacokinetics of bethanidine in hypertensive patients.

The pharmacolinetics of bethanidine-14C was studied in three hypertensive patients. A 25-MG DOSE OF BETHANIDINE-14 C hemisulfate was administered intravenously. Plasma levels of drug were measured over the first 6 hr. In 3 to 4 days, 89% to 94% of the dose was excreted in the urine. Thin-layer chromatography (TLC) and isotope dilution analysis of the urine samples indicated that only intact bethanidine was excreted. Plasma level and urinary excretion rate profiles had miltiphasic characteristics. Estimated half-lives of the terminal phase ranged from 7 to 11 hr. Average renal clearance over the initial 6 hr approached renal plasma flow. In 2 of the patients, renal clearance between 2 and 4 hr after administration was reduced to one-helf that observed during the initial 2-hr period. After single oral administration of a 25-mg dose of bethanidine-14C hemisulfate, 48% of 61% was excreted in urine and 15% to 48% in feces. Peak urinary excretion rates were reached 6 hr following administration. The urinary excretion kinetics of bethanidine during and after repetive oral dosing was also studied. A 25-mg dose was dividied into 12 to 16 equal doses and administered avery 6 hr. A larger fraction of the cumulative dose was recovered in the urine (72% to 74%) than after the single dose, suggesting higher availability at the lower dose. Steady-state urinary excretion rates were achieved in 4 to 7 doses. The steady-state urinary excretion levels were consistent with pharmacolinetic predictions based on single oral dose data. When 2 of the patients were given imipramine for 2 days prior to an oral 25-mg dose of bethanidine-14C hemisulfate, the terminal half-lives of the urinary excretion rate profiles were shorter than those in the same patients not given imipramine.

Administration, Oral↗
PubMed1975

Cycloalkanones V: synthesis, distribution, and effects on triglyceride metabolism.

The 14-C-labeled 2,8-dibenzylcyclooctanone was synthesized to study its absorption, distribution, and excretion in rats. Maximum drug absorption from the GI tract occurred between 12 and 14 hr after administration. The major organs possessed maximum amounts of the drug in 1 hr, with the liver concentrating the most with 6.56% 14-C and the muscle mass reaching a maximum of 41% 14-C after 14 hr. The drug remained in the GI tract over the first 6 hr and was associated with the lipid and glycogen fractions. Eighty-seven percent was eliminated in the feces after 72 hr. 2,8-Dibenzylcyclooctanone caused a significant reduction in vitro of dihydroxyacetone phosphatase acyltransferase and sn-glycerol-3-phosphate acyltransferase, which is the proposed mechanism for the observed in vivo reduction of hepatic, intestinal, and serum triglycerides and total glycerolipids. In vivo administration of the drug resulted in a depression of liver acid phosphatidyl phosphatase, acid phosphatase and lipase, and adipose lipase. The drug increased the rates of excretion of exogenous cholesterol, palmitic acid, and progesterone.

Acid Phosphatase↗
PubMed1975

Drug-biomolecule interactions: topographical study of active site of erythrocyte carbonic anhydrase using spin-labeled sulfanilamide drugs.

The topography of the active sites of human erythrocyte carbonic anhydrases B and C and bovine erythrocyte carbonic anhydrase B was studied using a series of spin-labeled sulfanilamide analogs. Results show that the active site of human carbonic anhydrase C is a narrow cleft approximately 14 A in depth. This observation is in good agreement with previously published X-ray diffraction data. While the active sites of human carbonic anhydrase B and bovine carbonic anhydrase B have the same general shape as the active site of human carbonic anhydrase C, they are slightly deeper.

Benzyl Compounds↗
PubMed1975

Electron-capture GLC determination of a new antiarrhythmic agent, alpha,alpha-dimethyl-4-(alpha,alpha,beta,beta-tetrafluorophenethyl) benzylamine, in biological fluids.

A highly specific and sensitive GLC method was developed for the analysis of alpha,alpha-dimethyl-4-(alpha,alpha,beta,beta-tetrafluorophenethyl) benzylamine, a new orally active antiarrhythmic drug, in biological fluids. The procedure involves the addition of an internal standard, 4-(alpha,alpha,beta,beta-tetrafluorophenethyl)benzylamine, to the plasma or urine samples followed by extraction of the drugs into benzene at pH 8. The extracted amines are converted to the trifluoroacetyl derivatives (characterized by GLG-mass spectrometry), chromatographed, and detected with a 63Ni electron-capture detector. The sensitivity of the method is such that 10 ng of alpha,alpha-dimethyl-4-(alpha,alpha,beta,beta-tetrafluorophenethyl)benzylamine/ml of plasma can be analyzed. These levels are suitable for the analysis of samples obtained following a therapeutic dose.

Animals↗
PubMed1975

High-pressure liquid chromatographic analysis of penicillin G potassium and its degradation products.

An anion-exchange high-pressure liquid chromatographic system capable of separating penicillin G potassium from five of its degradation products was developed. The retention times were: penicillin G potassium, 17.5 min; DL-penicillamine, 4.5 min; benzylpenilloic acid, 7.0 and 8.0 min; benzylpenamaldic acid, 13.0 min; benzylpenicilloic acid, 19.5 min; and benzylpenillic acid, 22.0 min. In addition, the system permits quantification using linear calibration curves.

Benzyl Compounds↗