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Biomedical subjects

F S Messiha

Publications and source records attributed to F S Messiha.

At least 163 records · Page 9Linked to original sources
PubMed1972

Peripheral aromatic L-amino acids decarboxylase inhibitor in Parkinsonism. I. Effect on O-methylated metabolites of L-dopa-2- 14 C.

The effects of MK-486, an inhibitor of peripheral aromatic L-amino acids decarboxylase, on the urinary metabolites derived from orally administered L-Dopa-2-(14)C were studied in three Parkinsonian patients. Treatment with MK-486 before L-Dopa-2-(14)C markedly reduced radioactivity found in catecholamines fraction by 70-80% during 48 hr, but increased 3-O-methyldopa fraction by threefold, as compared with a nonpretreated base line value. Pretreatment with MK-486 for a period of 1 wk resulted in less inhibition of O-methylated amine and acid metabolite fractions than that measured after a single dose of the inhibitor.

Aged↗
PubMedDate not supplied

d-Amphetamine and ethanol: a drug-drug interaction study.

The in vivo and in vitro effects of d-amphetamine on the specific activities of endogenous liver alcohol-(L-ADH) and aldehyde dehydrogenase (L-ADH) were studied using rat and mouse liver enzyme preparations. d-Amphetamine, 10(-4)M, noncompetitively inhibited rat and mouse L-ALDH in vitro. Mitochondrial L-ALDH was not affected by d-amphetamine in vivo and in vitro in both species studied. A noncompetitive inhibition of mouse L-ADH, occurred in vivo 16 hr after administration of d-amphetamine, 4 mg/kg, IP. A moderate, but not significant decline in specific activity of rat L-ADH was determined after injection of d-amphetamine, 4 mg/kg IP, showed a significant decrease in their blood and brain content of exogenously administered ethanol from corresponding saline-treated controls for the 60 min and 90 min periods after ethanol administration, respectively. The results show species differences in d-amphetamine action on liver enzymes studied and indicate that d-amphetamine can interfere in the metabolism of ethanol.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Taurine, analogues and ethanol elicited responses.

The effect of taurine, of some of its precursors and major metabolic products on spontaneous locomotor activity were studied in mice. The effect of taurine and some analogues on certain ethanol-mediated responses were observed. Administration of taurine, 50 mg/kg, IP, did not significantly alter motility in experimental animals compared to controls. Behavioral depression was evident subsequent to injection of cysteine hydrochloride or taurocholic acid (50 mg/kg). Administration of taurocholic acid, 50 mg/kg, IP, 30 min prior to a narcotic dose of ethanol, 5 g/kg, IP, reduced the time required for the onset of ethanol-narcosis. Pretreatment with cysteic acid, 50 mg/kg, IP, prolonged ethanol-produced narcosis. Treatment with cysteic acid 30 min prior to ethanol, 2.5 g/kg, IP, was found to decrease whole blood ethanol concentration as compared to the respective controls without a concomitant changes in brain ethanol levels. Administration of taurocholic acid, 100 mg/kg, IP, decreased the intake of an ethanol solution in rats preferring 5% ethanol solution over water as the drinking fluid of choice. None of the compounds tested altered endogenous specific activity of mouse liver alcohol dehydrogenase when given once daily (50 mg/kg, IP) for 10 consecutive days. The results suggest that both taurocholic acid and cysteic acid exert additive action to some ethanol-elicited responses studied.

Alcohol Drinking↗
PubMedDate not supplied

Effect of amantadine on motility of reserpinized mice as a function of brain biogenic amines and mouse strains.

The effect of amantadine, reserpine or both on locomotor activity and whole brain content of selected biogenic amines and major metabolites was studied as a function of mouse strain. Successive administration of small dose regimens of reserpine, 0.2 mg/kg IP, did not alter motility from corresponding saline control. Administration of amantadine, 100 mg/kg, IP, prior to each of the reserpine treatments produced either stimulation of motor activity in the albino ICR and black C57BL/6 mice or caused inhibition from reserpine in the albino BALB/C and the brown CDF-1 mouse strains. This suggests a genotype strain sensitivity to the amantadine and reserpine interaction on the motor behavior of the mouse. The amantadine treatment did not alter brain dopamine concentration but increased its immediate acid metabolite, 3,4-dihydroxyphenylacetic acid, in the C57BL/6 mice as contrasted with reduction of the same in the BALB/C mouse strain. Both BALB/C and C57BL/6 mice showed changes in brain normetanephrine levels as a consequence of the pharmacologic intervention used which suggest catecholaminergic sensitivity. The only changes produced by the agents studied in brain serotonin or 5-hydroxyindoleacetic acid levels were confined to the BALB/C mouse strain. No changes occurred in brain levels of the compounds measured from corresponding controls in the CDF-1 mice. The results indicate differential sensitivity of the serotonergic and dopaminergic systems to drug-drug interaction studied which appears to be strain dependent.

Amantadine↗
PubMedDate not supplied

Behavioral and metabolic aspects of cimetidine-ethanol interaction.

The effect of cimetidine, an H2 histamine receptor blocker, on spontaneous locomotor activity and ethanol-produced narcosis was studied in the male mouse. The separate and combined effects of cimetidine, and histalog (betazol), an H2 histamine receptor agonist, on voluntary intake of diluted ethanol solution by the rat were also determined. The in vitro effect of cimetidine on rat liver alcohol and aldehyde dehydrogenase was assayed. Cimetidine treatment was associated with an initial moderate increase in locomotor activity which was increased significantly as a function of time. The central depressant action of ethanol, as measured by duration of ethanol-mediated narcosis, was decreased by pretreatment with a single dose of cimetidine. The drug did not alter voluntary drinking of ethanol by the rat but antagonized histalog-produced aversion to ethanol selection when administered prior to histalog. Cimetidine, 3 x 10(-3) M concentration, inhibited rat liver aldehyde dehydrogenase but not alcohol dehydrogenase in vitro. The results indicate cimetidine-ethanol interaction and suggest the implication of histamine in some of the ethanol-elicited responses studied.

Animals↗
PubMedDate not supplied

Lithium and the neonate: developmental and metabolic aspects.

The interrelationship between lithium salts, which has been used in clinical trials of alcoholism, and ethanol, which evoke fetal alcohol syndrome by chronic use, was studied. This was made by evaluating the effect of prenatal and postnatal exposure to LiCl on ethanol and acetaldehyde metabolizing enzymes in the newborn mouse. The three Li-treatment regimens made consisted of acute and short-term prenatal exposure to LiCl in addition to postnatal exposure until weaning of the neonates. The weaned mice were then kept on water for a subsequent two weeks prior to sacrifice. The effects of LiCl, given in drinking fluid, on body weight, selected organ weights, hepatic alcohol dehydrogenase, aldehyde dehydrogenase and heart lactate dehydrogenase of the offspring were determined. Prenatal and postnatal ingestion of LiCl by the nursing mother resulted in decreased brain weight of offspring from both sexes. Concomitantly, there was a reduction in female but not male kidney weight. A marked decrease in the testis weight also occurred. The Li-treatment induced both neonatal hepatic alcohol dehydrogenase and heart lactate dehydrogenase in both sexes. Conversely, an inhibition of hepatic mitochondrial aldehyde dehydrogenase, for the enzyme with the apparent high Km, was determined in the male offspring. Maternal postnatal ingestion of LiCl decreased brain and spleen weights from corresponding control of neonatal male and female, respectively. This Li-treatment also induced hepatic neonatal alcohol dehydrogenase in both sexes. The results suggest that maternal ingestion of LiCl may interfere in brain development.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Dehydrogenase↗
PubMedDate not supplied

Alcohol withdrawal and carbamazepine.

The use of pharmacologic intervention in the management of alcohol withdrawal syndrome is briefly presented. The use of carbamazepine, a tricyclic anticonvulsant with clinical efficacy in depressive illness, in alcohol withdrawal treatment is reviewed. A comparative analysis between carbamazepine and major drugs used in alcohol withdrawal syndrome is made. This includes the evaluation of both clinical advantages and disadvantages in addition to identification of drug adverse reaction and interaction with alcohol. The mechanism of action of carbamazepine is also examined. Carbamazepine appears to possess a useful pharmacotherapeutic potential in the management of acute alcohol withdrawal syndrome, and its use in long-term treatment is suggested.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Carbamazepine and ethanol elicited responses in rodents.

The interaction between carbamazepine, and anticonvulsant with clinical efficacy in alcohol withdrawal syndrome, and ethanol was studied in rodents. Voluntary intake of ethanol by the rat was the behavioral performance test used to assess one aspect of such interaction. Carbamazepine, 50 mg/kg, IP, caused aversion to ethanol drinking. The drug was devoid of action on rat hepatic ethanol and acetaldehyde metabolizing enzymes, i.e., alcohol- and aldehyde dehydrogenase, and on testicular aldehyde dehydrogenase. The moderate induction of the latter by prolonged ethanol consumption was antagonized by a single dose of carbamazepine (50 mg/kg). Administration of carbamazepine, 50 mg/kg twice daily for three consecutive days, moderately inhibited mouse liver alcohol dehydrogenase in the male but not in the female mouse. This treatment did not alter endogenous mouse cardiac lactate dehydrogenase isoenzymes or hepatic aldehyde dehydrogenase in either sex. The enzymatic portion of the study suggests species and sex differences in the effects of carbamazepine studied. The reduction of voluntary drinking of ethanol by carbamazepine may have clinical implications, e.g., the extension of its use in alcohol withdrawal phase to alcohol abstinence.

Acetaldehyde↗
PubMedDate not supplied

Determination of carbamazepine by HPLC electrochemical detection and application for estimation of imipramine desipramine, doxepin and nordoxepin.

A simple analytical procedure for the estimation of carbamazepine in serum is presented. The procedure utilizes high pressure liquid chromatography with an electrochemical detection technique. The assay was also found applicable for the simultaneous separation of imipramine from desipramine or doxepin from nordoxepin. The procedure does not require the use of UV detection, is less time consuming and provides sensitivity at ng and microgram level for the tricyclic antidepressants studied and carbamazepine, respectively. This sensitivity is within the therapeutic range required for drug monitoring. The method is useful for the separation and quantitation of carbamazepine from imipramine and desipramine which is useful in cases where one of these drugs is given concurrently with carbamazepine.

Carbamazepine↗