Drugs online research references
Eur J Pharm Sci. 1999 Dec;9(2):221-5.
Spectrophotometric determination of some antidepressant drugs using 3-methylbenzothiazolin-2-one hydrazone.
Revanasiddappa HD, Manju B.
Department of Studies in Chemistry, University of Mysore, Manasagangothri, Mysore, India.
A sensitive spectrophotometric method for the determination of amitriptyline hydrochloride, nortriptyline hydrochloride and doxepin hydrochloride in pure and dosage forms, is described. The method is based on the oxidative coupling of the drugs with 3-methylbenzothiazolin-2-one hydrazone in the presence of iron(III) chloride in 1 M hydrochloric acid. The commonly encountered excipients and additives do not interfere with the determinations. Results of the present method are comparable with those of official methods. The new method offers the advantage of simplicity and rapidity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10620735&dopt=Abstract
Life Sci. 2000;66(3):271-8.
The inhibition of GLUT1 glucose transport and cytochalasin B binding activity by tricyclic antidepressants.
Pinkofsky HB, Dwyer DS, Bradley RJ.
Department of Psychiatry, Louisiana State University Health Sciences Center, Shreveport 71130-3932, USA.
Under normal metabolic conditions glucose is an important energy source for the mammalian brain. Positron Emission Tomography studies of the central nervous system have demonstrated that tricyclic antidepressant medications alter cerebral metabolic function. The mode by which these drugs perturb metabolism is unknown. In the present study the interactions of tricyclic antidepressants with the GLUT1 glucose transport protein is examined. Amitriptyline, nortriptyline, desipramine, and imipramine all inhibit the influx of 3-O-methyl glucose into resealed erythrocytes. This inhibition is observed with drug concentrations in the millimolar range. All four antidepressants also noncompetitively displace cytochalasin B binding to GLUT1. The K(I) for this displacement ranges from 0.56 to 1.43 millimolar. This value is in a range greater than that associated with clinical doses and this effect may not be directly applicable to side effects observed with normal use. The observed interaction of these drugs with GLUT1 may reflect an affinity for other glucose-transport or glucose-binding proteins, and may possibly contribute to tricyclic antidepressant toxicity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10666003&dopt=Abstract
Brain Res. 2000 Feb 14;855(2):235-43.
Cytochrome P-450 activities in human and rat brain microsomes.
Voirol P, Jonzier-Perey M, Porchet F, Reymond MJ, Janzer RC, Bouras C, Strobel HW, Kosel M, Eap CB, Baumann P.
Unite de Biochimie et Psychopharmacologie Clinique, Departement Universitaire de Psychiatrie Adulte, CH-1008 Prilly, Lausanne, Switzerland.
The role of cytochrome P450 in the metabolism of dextromethorphan, amitriptyline, midazolam, S-mephenytoin, citalopram, fluoxetine and sertraline was investigated in rat and human brain microsomes. Depending on the parameters, the limit of quantification using gas chromatography-mass spectrometry methods was between 1.6 and 20 pmol per incubation, which generally contained 1500 microg protein. Amitriptyline was shown to be demethylated to nortriptyline by both rat and human microsomes. Inhibition studies using ketoconazole, furafylline, sulfaphenazole, omeprazole and quinidine suggested that CYP3A4 is the isoform responsible for this reaction whereas CYP1A2, CYP2C9, CYP2C19 and CYP2D6 do not seem to be involved. This result was confirmed by using a monoclonal antibody against CYP3A4. Dextromethorphan was metabolized to dextrorphan in rat brain microsomes and was inhibited by quinidine and by a polyclonal antibody against CYP2D6. Only the addition of exogenous reductase allowed the measurement of this activity in human brain microsomes. Metabolites of the other substrates could not be detected, possibly due to an insufficiently sensitive method. It is concluded that cytochrome P450 activity in the brain is very low, but that psychotropic drugs could undergo a local cerebral metabolism which could have pharmacological and/or toxicological consequences.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10677595&dopt=Abstract
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