Plasma Dopamine-Beta-Hydroxylase and Platelet Monoamine Oxidase
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Food and Mood: Eating Plants to Fight the Blues P H Y S I C I a N S C O M M I T T E E F O R R E S P O N S I B L E M E D I C I N E 5 1 0 0 W I S C O N S I N a V E., N
Food and Mood: Eating Plants to Fight the Blues P H Y S I C I A N S C O M M I T T E E F O R R E S P O N S I B L E M E D I C I N E 5 1 0 0 W I S C O N S I N A V E., N. W., S U I T E 4 0 0 • W A S H I N G T O N, D C 2 0 0 1 6 P H O N E ( 2 0 2 ) 6 8 6 - 2 2 1 0 • F A X ( 2 0 2 ) 6 8 6 - 2 2 1 6 • P C R M @ P C R M . O R G • W W W . PHYSICIANSCOMMITTEE . O R G suffering from depression have elevated levels of an enzyme called monoamine oxidase (MAO).4 This enzyme breaks down serotonin, dopamine, and norepinephrine—neurotransmitters which help regulate mood. High MAO levels lead to low levels of these specific neurotransmitters, causing depression. The phytochemical quercetin, found only in plant foods, acts as an MAO inhibitor.5 Working much like a natural antidepressant, quercetin can increase the amount of serotonin, dopamine, and norepinephrine in the brain. Foods with high levels of quercetin include apples, kale, berries, grapes, onion, and green tea.6 Arachidonic acid, a type of fat found only in animals, serves as a precursor to inflammatory chemicals in our bodies. By eating foods high in arachidonic acid, such as chicken, eggs, and other animal products, we set off a cascade of chemical reactions in our body. -
Catecholamines and the Hydroxylation of Tyrosine in Synaptosomes Isolated from Rat Brain (DOPA/Tyramine/Dopamine/Norepinephrine/Octopamine) M
Proc. Nat. Acad. Sci. USA Vol. 68, No. 10, pp. 2370-2373, October 1971 Catecholamines and the Hydroxylation of Tyrosine in Synaptosomes Isolated from Rat Brain (DOPA/tyramine/dopamine/norepinephrine/octopamine) M. KAROBATH Psychiatric Research Laboratories, Massachusetts General Hospital, Boston, Mass. 02114 Communicated by Seymour S. Kety, July 16, 1971 ABSTRACT Tyrosine hydroxylase activity of synapto- removing transmitters from an extraneuronal location at the somes isolated from rat brain was examined. A modified synapse, then incubation of synaptosomes with catechol- tritium-displacement assay was used, which allowed the measurement of tyrosine hydroxylase activity without the amines should inhibit the formation of DOPA from tyrosine. addition of either inhibitors of the metabolism of the The experiments demonstrate that tyrosine hydroxylase hydroxylated products or added exogenous cofactor. The activity is affected by catecholamine uptake. The concentra- enzyme activity was strongly inhibited by the addition of tions required to inhibit the synthesis of catechols are in the exogenous catecholamines and 3,4-dihydroxy-L-phenyl- M. alanine. Aromatic amines other than catechols did not range of 10-7 markedly influence tyrosine hydroxylase activity. These MATERIALS AND METHODS in vitro findings support the hypothesis that synthesis of catecholamines is regulated by a mechanism of end- [3,5-H]HifTyrosine (Tracerlab) was purified by column chro- product inhibition at the tyrosine hydroxylase step. matography. Catechol impurities were absorbed on alumina and tritiated water and anions were removed by Synaptosomes are pinched-off nerve endings with relatively columns (8), by non-neuronal elements (1, 2). They absorption on Dowex-50 resin. Tyrosine was eluted from little contamination Dowex-50 with 25 ml of 4 N HCl; after distillation of the eluate contain the enzymes necessary for the synthesis of dopamine (v/v) from tyrosine (3, 4). -
Oxoglutarate Dehydrogenase Multienzyme Complexes Reconstituted from Recombinant
*RevisedView metadata, Manuscript citation and (text similar UNmarked) papers at core.ac.uk brought to you by CORE Click here to view linked References provided by Repository of the Academy's Library Formation of reactive oxygen species by human and bacterial pyruvate and 2- oxoglutarate dehydrogenase multienzyme complexes reconstituted from recombinant components Attila Ambrusa, Natalia S. Nemeriab, Beata Torocsika, Laszlo Trettera, Mattias Nilssona, Frank Jordanb, and Vera Adam-Vizia,* aDepartment of Medical Biochemistry, MTA-SE Laboratory for Neurobiochemistry, Semmelweis University, Budapest, 1094, Hungary bDepartment of Chemistry, Rutgers, the State University, Newark, NJ 07102, USA *To whom correspondence should be addressed at: Department of Medical Biochemistry, Semmelweis University, 37-47 Tuzolto Street, Budapest, 1094, Hungary. Tel.: +361 266 2773, Fax.: +361 267 0031, E-mail: [email protected] 1 Abstract Individual recombinant components of pyruvate and 2-oxoglutarate dehydrogenase multienzyme complexes (PDHc, OGDHc) of human and Escherichia coli (E. coli) origin were expressed and purified from E. coli with optimized protocols. The four multienzyme complexes were each reconstituted under optimal conditions at different stoichiometric ratios. Binding stoichiometries for the highest catalytic efficiency were determined from the rate of NADH generation by the complexes at physiological pH. Since some of these complexes were shown to possess ‘moonlighting’ activities under pathological conditions often accompanied by acidosis, activities were also determined at pH 6.3. As reactive oxygen species (ROS) generation by the E3 component of hOGDHc is a pathologically relevant feature, superoxide generation by the complexes with optimal stoichiometry was measured by the acetylated cytochrome c reduction method in both the forward and the reverse catalytic directions. -
Phenelzine Switching Advice 11 May 2020
Mental Health Special Interest Group Guidance for switching from phenelzine to another antidepressant The supplier of phenelzine sulphate tablets has notified PHARMAC that they can no longer supply this medication in New Zealand. This is reportedly a global issue so the supplier can no longer guarantee supply of any brand of phenelzine. Supplies of phenelzine tablets are likely to run out by mid-late May 2020. People taking phenelzine should be reviewed and, if appropriate, transitioned to another antidepressant as soon as possible. Phenelzine is a non-selective and irreversible monoamine oxidase inhibitor (MAOI) of the hydrazine class. The only remaining non-selective irreversible MAOI available in New Zealand is tranylcypromine. Tranylcypromine is a non-hydrazine MAOI and differs significantly from phenelzine in some aspects, as outlined below. Tranylcypromine may be an appropriate alternative antidepressant for some patients ; however, it is important to consider an individual’s physical health and psychiatric history, and whether an MAOI is still appropriate. General practitioners should consult with a psychiatrist regarding treatment options and transition. Reducing and stopping phenelzine The dose of phenelzine should ideally be tapered down over a minimum of four weeks, starting immediately in light of very limited supplies. We acknowledge that a faster taper may be required in some cases due to rapidly declining stock. Irreversible MAOIs are associated with a high risk of discontinuation symptoms, e.g. nightmares, headache, irritability, feeling cold, disorientation, hypomania, nausea, sweating, palpitations, myoclonic jerks and, rarely, catatonia or psychosis. Significant discontinuation symptoms should be closely monitored and managed in consultation with a psychiatrist. It is important to maintain MAOI dietary and co-prescribed medication precautions for at least 14 days after stopping phenelzine. -
Genetic and Proteinic Linkage of MAO and COMT with Oral Potentially Malignant Disorders and Cancers of the Oral Cavity and Pharynx
cancers Article Genetic and Proteinic Linkage of MAO and COMT with Oral Potentially Malignant Disorders and Cancers of the Oral Cavity and Pharynx Ping-Ho Chen 1,2,3,4,5,6 , Yen-Yun Wang 1,4,5, Ting-Hsun Lan 1,7 , Leong-Perng Chan 6,8,9 and Shyng-Shiou Yuan 4,5,10,11,12,13,* 1 School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan; [email protected] (P.-H.C.); [email protected] (Y.-Y.W.); [email protected] (T.-H.L.) 2 Institute of Biomedical Sciences, National Sun Yat-Sen University, No. 70 Lienhai Road, Kaohsiung 804201, Taiwan 3 Department of Veterinary Medicine, College of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung 912301, Taiwan 4 Center for Cancer Research, Kaohsiung Medical University, Kaohsiung 807378, Taiwan 5 Cancer Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 807378, Taiwan 6 Cohort Research Center, Kaohsiung Medical University, Kaohsiung 807378, Taiwan; [email protected] 7 Division of Prosthodontics, Department of Dentistry, Kaohsiung Medical University Hospital, Kaohsiung 807378, Taiwan 8 Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan 9 Department of Otorhinolaryngology-Head and Neck Surgery, Kaohsiung Municipal Ta-Tung Hospital and Citation: Chen, P.-H.; Wang, Y.-Y.; Kaohsiung Medical University Hospital, Kaohsiung 807378, Taiwan Lan, T.-H.; Chan, L.-P.; Yuan, S.-S. 10 Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung 807378, Taiwan Genetic and Proteinic Linkage of 11 Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, MAO and COMT with Oral Kaohsiung 807378, Taiwan 12 Potentially Malignant Disorders and Translational Research Center, Kaohsiung Medical University Hospital, Kaohsiung 807378, Taiwan 13 Cancers of the Oral Cavity and Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Pharynx. -
Serotonin Syndrome Due to Co-Administration of Linezolid and Methadone
Le Infezioni in Medicina, n. 3, 263-266, 2017 CASE REPORT 263 Serotonin syndrome due to co-administration of linezolid and methadone Antonio Mastroianni1, Gianfranco Ravaglia2 1U.O. Malattie Infettive, Presidio Ospedaliero, “G.B. Morgagni - L. Pierantoni”, Forlì, Italy; 2U.O. Farmacia, Presidio Ospedaliero “G.B. Morgagni - L. Pierantoni”, Forlì, Italy SUMMARY Serotonin syndrome (SS), a potentially life-threatening verity from mild to life-threatening. To our knowledge, adverse drug reaction caused by excessive serotoner- we present the first reported case of SS associated with gic agonism in central and peripheral nervous system linezolid and methadone with a brief review of the lit- serotonergic receptors, may be caused by a single drug erature. or a combination of drugs with serotonergic activity. The syndrome results in a variety of mental, autonom- Keywords: serotonin syndrome, linezolid, methadone, ic and neuromuscular changes, which can range in se- methicillin-resistant Staphylococcus aureus. n INTRODUCTION methadone. This serious adverse interaction be- tween linezolid and methadone inducing SS was erotonin syndrome (SS) is a toxic state caused reported in a drug-addict HIV-positive man with Smainly by excessive serotonergic activity in sepsis, osteomyelitis and multiple muscle abscess- the nervous system, nearly always caused by a es and metastatic skin abscesses caused by meth- drug interaction involving two or more “seroto- icillin-resistant Staphylococcus aureus (MRSA), un- nergic” drugs [1]. These include serotonin pre- der combined antibiotic treatment. cursors, serotonin agonists, serotonin releasers, serotonin reuptake inhibitors, monoaminoxidase inhibitors (MAOIs) and some herbal medicines. n CASE REPORT Linezolid is a weak, nonselective, reversible in- hibitor of MAOIs, and potentially may interact A 39-year-old drug-addict male was admitted to with MAOIs and adrenergic and serotonergic our department with fever (up to 39.5°C) and a agents. -
BY B. JARROTT* and S. Z. Langert from the Department of Pharmacology, University of Cambridge, and the Agricultural Research
J. Physiol. (1971), 212, pp. 549-559 549 With 2 text-figure8 Printed in Great Britain CHANGES IN MONOAMINE OXIDASE AND CATECHOL-O-METHYL TRANSFERASE ACTIVITIES AFTER DENERVATION OF THE NICTITATING MEMBRANE OF THE CAT BY B. JARROTT* AND S. Z. LANGERt From the Department of Pharmacology, University of Cambridge, and the Agricultural Research Council, Institute of Animal Physiology, Babraham, Cambridge (Received 10 August 1970) SUMMARY 1. The question of cellular localizations of monoamine oxidase and catechol-o-methyl transferase, enzymes involved in the metabolism of noradrenaline, has been investigated by following the changes in the enzyme activity of the smooth muscle of the cat nictitating membrane after sympathetic denervation. Any falls in enzyme activity coinciding with the time course for degeneration of the sympathetic nerve endings (2-3 days) can reasonably be ascribed to a former localization of the enzyme within the sympathetic nerve. 2. Monoamine oxidase activity of the inferior and medial smooth muscle was significantly reduced 3 days after sympathectomy and re- mained reduced 14 days after sympathectomy. 3. A correlation was found between the fall in monoamine oxidase activity and the endogenous noradrenaline concentration of the contra- lateral normal muscle, indicating that the higher the endogenous nor- adrenaline concentration, the greater the fall in monoamine oxidase activity after denervation. 4. It was concluded that the fall in monoamine oxidase activity after denervation indicated a former localization of the enzyme within the sympathetic nerve endings. 5. The fall in monoamine oxidase activity of the denervated muscle was significantly less measured with benzylamine as a substrate than with tyramine. -
04A-Agents of Synaptic Transmission
10/22/2009 Agents of Synaptic Transmission Mary ET Boyle, Ph.D. Department of Cognitive Science UCSD Agents of Synaptic Transmission: SmallSmall--MoleculeMolecule Neurotransmitters Amino acids ◦ glutamate ◦ gamma-amino butyric acid (GABA) ◦ aspartate ◦ glycine Monoamines ◦ catecholamines epinephrine (adrenalin) norepinephrine (noradrenalin) dopamine ◦ indoleamines serotonin melatonin 1 10/22/2009 Agents of Synaptic Transmission: SmallSmall--MoleculeMolecule Neurotransmitters Soluble gases ◦ nitric oxide ◦ carbon monoxide Acetylcholine Agents of Synaptic Transmission: LargeLarge--MoleculeMolecule Neurotransmitters endogenous opioids substance P oxytocin antidiuretic hormone (ADH) cholecystokinin (CCK) 2 10/22/2009 Glutamate Glutamate is the most common excitatory neurotransmitter in the CNS. Synapses that use glutamate are called glutamatergic. Termination of action is byyp reuptake. Implicated in Huntington’s disease. Extreme anxiety, linked to below normal GABA levels, may be treated with Valium. Appears to be involved with memory storage and retrieval. GABAergic Synapse GammaGamma--aminobutricaminobutricacid most common inhibitory transmitter in the brain Its synapses are called GABAergic and it is terminated by reuptake. 3 10/22/2009 monoamines catecholamines dopamine norepinephrine epinephrine in the brain Monoamines: cateholamines and indoleamines Catecholamines ◦ Norepinephrine (NE) NE transmission is called adrenergic. NE is terminated by reuptake and degrad ation of NE within the cytoplasm, not in synaptic vesicles, by monoamine oxidase (MAO). NE is the transmitter in the sympathetic nervous system and is involved in regulating attention, concentration, arousal, sleep and depression. ◦ Dopamine (DA) A precursor to NE. Found in the substantia nigra and basal ganglia Involved in voluntary movements, schizophrenia, Parkinson’s disease, and addictions including nicotine, alcohol and others 4 10/22/2009 Neurons using …. Neurons using dopamine are called “dopaminergic.” Neurons using epinephrine are called “adrenergic”. -
Role of Monoamine Oxidase Activity in Alzheimer's Disease
molecules Review Role of Monoamine Oxidase Activity in Alzheimer’s Disease: An Insight into the Therapeutic Potential of Inhibitors Tapan Behl 1,*, Dapinder Kaur 1, Aayush Sehgal 1, Sukhbir Singh 1, Neelam Sharma 1, Gokhan Zengin 2, Felicia Liana Andronie-Cioara 3 , Mirela Marioara Toma 4,5, Simona Bungau 4,5,* and Adrian Gheorghe Bumbu 6 1 Department of Pharmacology, Chitkara College of Pharmacy, Chitkara University, Rajpura 140401, Punjab, India; [email protected] (D.K.); [email protected] (A.S.); [email protected] (S.S.); [email protected] (N.S.) 2 Department of Biology, Faculty of Science, Selcuk University Campus, 42130 Konya, Turkey; [email protected] 3 Department of Psycho-Neuroscience and Recovery, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania; [email protected] 4 Department of Pharmacy, Faculty of Medicine and Pharmacy, University of Oradea, 410028 Oradea, Romania; [email protected] 5 Doctoral School of Biomedical Sciences, University of Oradea, 410073 Oradea, Romania 6 Department of Surgical Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania; [email protected] * Correspondence: [email protected] (T.B.); [email protected] (S.B.) Abstract: Despite not being utilized as considerably as other antidepressants in the therapy of Citation: Behl, T.; Kaur, D.; Sehgal, depression, the monoamine oxidase inhibitors (MAOIs) proceed to hold a place in neurodegeneration A.; Singh, S.; Sharma, N.; Zengin, G.; and to have a somewhat broad spectrum in respect of the treatment of neurological and psychiatric Andronie-Cioara, F.L.; Toma, M.M.; conditions. Preclinical and clinical studies on MAOIs have been developing in recent times, especially Bungau, S.; Bumbu, A.G. -
Monoamine Oxidase a Deficiency
Monoamine oxidase A deficiency Description Monoamine oxidase A deficiency is a rare disorder that occurs almost exclusively in males. It is characterized by mild intellectual disability and behavioral problems beginning in early childhood. Most boys with monoamine oxidase A deficiency are less able to control their impulses than their peers, causing aggressive or violent outbursts. In addition, affected individuals may have features of other behavioral disorders, including autism spectrum disorder and attention-deficit/hyperactivity disorder (ADHD). These features can include obsessive behaviors, difficulty forming friendships, and problems focusing attention. Sleep problems, such as trouble falling asleep or night terrors, can also occur in monoamine oxidase A deficiency. Some people with monoamine oxidase A deficiency have episodes of skin flushing, sweating, headaches, or diarrhea. Similar episodes can occur in female family members of males with monoamine oxidase A deficiency, although females do not experience other signs or symptoms of the condition. In some cases, certain foods, such as cheese, appear to worsen symptoms of monoamine oxidase A deficiency. Frequency Monoamine oxidase A deficiency is thought to be very rare. Its prevalence is unknown. Causes Monoamine oxidase A deficiency is caused by mutations in the MAOA gene. This gene provides instructions for making an enzyme called monoamine oxidase A. This enzyme breaks down chemicals called monoamines, including serotonin, epinephrine, and norepinephrine. These particular monoamines act as neurotransmitters, which transmit signals between nerve cells in the brain. Monoamine oxidase A helps break down the neurotransmitters when signaling is no longer needed. Signals transmitted by serotonin regulate mood, emotion, sleep, and appetite. Epinephrine and norepinephrine control the body's response to stress. -
Profiling of Tryptophan Metabolic Pathways in the Rat Fetoplacental
International Journal of Molecular Sciences Article Profiling of Tryptophan Metabolic Pathways in the Rat Fetoplacental Unit during Gestation 1, 1, 2 1 1 Cilia Abad y, Rona Karahoda y , Petr Kastner , Ramon Portillo , Hana Horackova , Radim Kucera 2, Petr Nachtigal 3 and Frantisek Staud 1,* 1 Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University, Akademika Heyrovskeho 1203, 500 05 Hradec Kralove, Czech Republic; [email protected] (C.A.); [email protected] (R.K.); [email protected] (R.P.); [email protected] (H.H.) 2 Department of Pharmaceutical Chemistry and Pharmaceutical Analysis, Faculty of Pharmacy in Hradec Kralove, Charles University, Akademika Heyrovskeho 1203, 500 05 Hradec Kralove, Czech Republic; [email protected] (P.K.); [email protected] (R.K.) 3 Department of Biological and Medical Sciences, Faculty of Pharmacy in Hradec Kralove, Charles University, Akademika Heyrovskeho 1203, 500 05 Hradec Kralove, Czech Republic; [email protected] * Correspondence: [email protected]; Tel.: +420-495-067-407 These authors contributed equally to this work. y Received: 23 September 2020; Accepted: 11 October 2020; Published: 14 October 2020 Abstract: Placental homeostasis of tryptophan is essential for fetal development and programming. The two main metabolic pathways (serotonin and kynurenine) produce bioactive metabolites with immunosuppressive, neurotoxic, or neuroprotective properties and their concentrations in the fetoplacental unit must be tightly regulated throughout gestation. Here, we investigated the expression/function of key enzymes/transporters involved in tryptophan pathways during mid-to-late gestation in rat placenta and fetal organs. Quantitative PCR and heatmap analysis revealed the differential expression of several genes involved in serotonin and kynurenine pathways. -
TASMAR® (Tolcapone) TABLETS
TASMAR® (tolcapone) TABLETS Before prescribing TASMAR, the physician should be thoroughly familiar with the details of this prescribing information. TASMAR SHOULD NOT BE USED BY PATIENTS UNTIL THERE HAS BEEN A COMPLETE DISCUSSION OF THE RISKS AND THE PATIENT HAS PROVIDED WRITTEN ACKNOWLEDGEMENT THAT THE RISKS HAVE BEEN EXPLAINED (SEE PATIENT ACKNOWLEDGEMENT OF RISKS SECTION). WARNING: Because of the risk of potentially fatal, acute fulminant liver failure, TASMAR (tolcapone) should ordinarily be used in patients with Parkinson’s disease on l- dopa/carbidopa who are experiencing symptom fluctuations and are not responding satisfactorily to or are not appropriate candidates for other adjunctive therapies (see INDICATIONS and DOSAGE AND ADMINISTRATION sections). Because of the risk of liver injury and because TASMAR, when it is effective, provides an observable symptomatic benefit, the patient who fails to show substantial clinical benefit within 3 weeks of initiation of treatment, should be withdrawn from TASMAR. TASMAR therapy should not be initiated if the patient exhibits clinical evidence of liver disease or two SGPT/ALT or SGOT/AST values greater than the upper limit of normal. Patients with severe dyskinesia or dystonia should be treated with caution (see PRECAUTIONS: Rhabdomyolysis). PATIENTS WHO DEVELOP EVIDENCE OF HEPATOCELLULAR INJURY WHILE ON TASMAR AND ARE WITHDRAWN FROM THE DRUG FOR ANY REASON MAY BE AT INCREASED RISK FOR LIVER INJURY IF TASMAR IS REINTRODUCED. ACCORDINGLY, SUCH PATIENTS SHOULD NOT ORDINARILY BE CONSIDERED FOR RETREATMENT. Cases of severe hepatocellular injury, including fulminant liver failure resulting in death, have been reported in postmarketing use. As of May 2005, 3 cases of fatal Reference ID: 3307244 fulminant hepatic failure have been reported from more than 40,000 patient years of worldwide use.