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Rotzinger, Susan; Bourin, Michel; Akimoto, Yoshio; Coutts, Ronald T.; Baker, Glen B.

doi:10.1023/a:1006953923305

Cited by 206 publications

(6 citation statements)

References 86 publications

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“…Taken together, it appears that baboon hepatic and placental 11β-HSD, carbonyl reductases and to a lesser extent aldo-ketoreductases are responsible for the reduction of the carbonyl group of bupropion to threo- and erythrohydrobupropion. This is in agreement with the report demonstrating that carbonyl-reducing enzymes are involved in the biotransformation of bupropion to threo- and erythrohydrobupropion by human placental microsomes [5]. Furthermore, the similarities between human and baboon placental 11β-HSD in catalyzing the metabolism of cortisol and cortisone has been also reported [34].…”

Section: Discussionsupporting

confidence: 91%

“…Additionally, the onset of pregnancy is accompanied by changes in maternal physiology that affect the absorption, distribution, metabolism, and elimination of administered medications [4]. In humans, bupropion is extensively metabolized in vivo and less than 10% of the drug is excreted unchanged in urine and feces [5, 6]. Furthermore, recent preclinical data obtained from in vitro studies revealed that bupropion is also metabolized by human placenta [7].…”

Section: Introductionmentioning

confidence: 99%

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Metabolism of bupropion by baboon hepatic and placental microsomes

Wang

Abdelrahman

Fokina

et al. 2011

Biochemical Pharmacology

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The aim of this investigation was to determine the biotransformation of bupropion by baboon hepatic and placental microsomes, identify the enzyme(s) catalyzing the reaction(s) and determine its kinetics. Bupropion was metabolized by baboon hepatic and placental microsomes to hydroxybupropion (OH-BUP), threo- (TB) and erythrohydrobupropion (EB). OH-bupropion was the major metabolite formed by hepatic microsomes (Km 36 ± 6 µM, Vmax 258 ± 32 pmol mg protein−1 min−1), however the formation of OH-BUP by placental microsomes was below the limit of quantification. The apparent Km values of bupropion for the formation of TB and EB by hepatic and placental microsomes were similar. The selective inhibitors of CYP2B6 (ticlopidine and phencyclidine) and monoclonal antibodies raised against human CYP2B6 isozyme caused 80% inhibition of OH-BUP formation by baboon hepatic microsomes. The chemical inhibitors of aldo-keto reductases (flufenamic acid), carbonyl reductases (menadione), and 11β-hydroxysteroid dehydrogenases (18β-glycyrrhetinic acid) significantly decreased the formation of TB and EB by hepatic and placental microsomes. Data indicate that CYP2B of baboon hepatic microsomes is responsible for biotransformation of bupropion to OH-BUP, while hepatic and placental short chain dehydrogenases/reductases and to a lesser extent aldo-keto reductases are responsible for the reduction of bupropion to TB and EB.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Metabolism of bupropion by baboon hepatic and placental microsomes

Wang

Abdelrahman

Fokina

et al. 2011

Biochemical Pharmacology

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“…Cytochrome P3A4 mediates the N -dealkylation that results in the formation of the active metabolite 1- m -chlorophenylpiperazine, which then undergoes hydroxylation by CYP2D6. 96 Therapeutic response has been associated with plasma trazodone concentrations of approximately 700 ng/mL but not with 1- m -chlorophenylpiperazine 97 plasma levels. Cytochrome P1A2 may also be involved in trazodone metabolism.…”

Section: Resultsmentioning

confidence: 99%

Pharmacotherapy for Mood Disorders in Pregnancy

Deligiannidis¹,

Byatt

Freeman³

2014

Journal of Clinical Psychopharmacology

164

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Objective Pharmacotherapy for mood disorders during pregnancy is often complicated by pregnancy-related pharmacokinetic changes and the need for dose adjustments. The objectives of this review are to summarize the evidence for change in perinatal pharmacokinetics of commonly used pharmacotherapies for mood disorders, discuss the implications for clinical and therapeutic drug monitoring (TDM), and make clinical recommendations. Methods The English-language literature indexed on MEDLINE/PubMed was searched for original observational studies (controlled and uncontrolled, prospective and retrospective), case reports, and case series that evaluated or described pharmacokinetic changes or TDM during pregnancy or the postpartum period. Results Pregnancy-associated changes in absorption, distribution, metabolism, and elimination may result in lowered psychotropic drug levels and possible treatment effects, particularly in late pregnancy. Mechanisms include changes in both phase 1 hepatic cytochrome P450 and phase 2 uridine diphosphate glucuronosyltransferase enzyme activities, changes in hepatic and renal blood flow, and glomerular filtration rate. Therapeutic drug monitoring, in combination with clinical monitoring, is indicated for tricyclic antidepressants and mood stabilizers during the perinatal period. Conclusions Substantial pharmacokinetic changes can occur during pregnancy in a number of commonly used antidepressants and mood stabilizers. Dose increases may be indicated for antidepressants including citalopram, clomipramine, imipramine, fluoxetine, fluvoxamine, nortriptyline, paroxetine, and sertraline, especially late in pregnancy. Antenatal dose increases may also be needed for lithium, lamotrigine, and valproic acid because of perinatal changes in metabolism. Close clinical monitoring of perinatal mood disorders and TDM of tricyclic antidepressants and mood stabilizers are recommended.

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“…[550] Conversely, ketoconazole, fluconazole, itraconazole and terbinafine themselves are potent inhibitors of the CYP 3A4 isoenzyme, which is responsible for the metabolism of TCAs,[3] trazodone[70] and carbamazepine. [10225167] As a consequence, the plasma concentrations of TCAs and carbamazepine may rise and reach toxic levels.…”

Section: Resultsmentioning

confidence: 99%

Antidepressants relevant to oral and maxillofacial surgical practice

Lambrecht

Greuter

Surber

2013

Ann Maxillofac Surg

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Background:Depression is commonly associated with a high-carbohydrate diet, lack of interest in proper oral hygiene and xerostomia connected to the use of antidepressants. Patients often consult their dentists as a result of changes affecting the hard dental substance and the soft-tissues.Aim:The aim of this study was to identify adverse drug interactions between the antidepressants and medications commonly administered in dentistry in order to give practicing dentists an overview of the scientific literature.Objective:The objective is to identify the adverse drug interactions between antidepressants and medication commonly administered in dentistry.Study Design:The literature search was performed using PubMed, Cochrane and the specific search items. The review (1984-2009) focused on medicines used in dental practice (vasoconstrictors, non-opioid analgesics, non-steroidal anti-inflammatory drugs, antibiotics, antifungals and benzodiazepines).Results:There are various drug interactions between antidepressants and medicines used in dentistry. When two or more drugs are co-administered, a drug interaction must always be anticipated though many of the interactions are potential problems, but do not seem to be real clinical issues.Conclusion:The probability of a drug interaction can be minimized by careful history-taking, skillful dose adjustment and safe administration of the therapeutic agent.

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Untitled

Cited by 206 publications

References 86 publications

Metabolism of bupropion by baboon hepatic and placental microsomes

Metabolism of bupropion by baboon hepatic and placental microsomes

Pharmacotherapy for Mood Disorders in Pregnancy

Antidepressants relevant to oral and maxillofacial surgical practice

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