儿茶酚氧位甲基转移酶与疾病的关系
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摘要
儿茶酚氧位甲基转移酶(COMT)是内源基因表达的二相代谢酶,由22号染色体表达。主要将S-腺苷甲硫氨酸上的甲基转移至底物的羟基上,使底物的一个羟基甲基化。COMT在体内的主要作用是代谢儿茶酚类的化合物,例如:多巴胺、肾上腺素、去甲肾上腺素、雌二醇等化合物,此外还能代谢体外通过饮食及药物摄入的儿茶酚类化合物。由于COMT在体内与化合物的代谢密切相关,COMT代谢失常能够引起很多疾病或者罹患疾病的风险增加,例如:帕金森病、精神分裂症、乳腺癌等疾病。本综述通过阐述COMT代谢紊乱引起的疾病尝试说明COMT与其相关疾病之间的联系,旨在能够对COMT代谢相关疾病提供有效的治疗方法。
Catechol O-methyltransferase(COMT), one of the endogenous phase II metabolizing enzymes, expressed by chromosome 22. COMT catalyzes the transfer of a methyl group from common methyl donor S-adenosyl-L-methionine(Ado Met or SAM) to one of the catechol hydroxyls. COMT participates in the metabolism of many catechols in vivo, e.g. dopamine, epinephrine, noradrenaline, estradiol. Furthermore COMT also plays important roles in the metabolism of xenobiotic catechols from food and drug. COMT play a critical role in the management of catechols. Metabolism disorders of COMT can cause many diseases or an increased risk of diseases, e.g. Pakinson diseases, schizophrenia, and breast cancer. In this review, we explains the relationship of COMT and related-diseases through expounding disease caused by the COMT metabolic disorders. Finally, we hope that there will be more effective treatments for the COMT metabolism related diseases.
Catechol O-methyltransferase(COMT), one of the endogenous phase II metabolizing enzymes, expressed by chromosome 22. COMT catalyzes the transfer of a methyl group from common methyl donor S-adenosyl-L-methionine(Ado Met or SAM) to one of the catechol hydroxyls. COMT participates in the metabolism of many catechols in vivo, e.g. dopamine, epinephrine, noradrenaline, estradiol. Furthermore COMT also plays important roles in the metabolism of xenobiotic catechols from food and drug. COMT play a critical role in the management of catechols. Metabolism disorders of COMT can cause many diseases or an increased risk of diseases, e.g. Pakinson diseases, schizophrenia, and breast cancer. In this review, we explains the relationship of COMT and related-diseases through expounding disease caused by the COMT metabolic disorders. Finally, we hope that there will be more effective treatments for the COMT metabolism related diseases.
引文
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[2]Axelrod J,Tomchick R.Enzymatic O-methylation of epinephrine and other catechols[J].J Biol Chem,1958,233:702-705.
[3]Grossman MH,Emanuel BS,Budarf ML.Chromosomal mapping of the human catechol-O-methyltransferase gene to22q11.1→q11.2[J].Genomics,1992,12:822-825.
[4]Lundstrom K,Tenhunen J,Tilgmann C,et al.Cloning,expression and structure of catechol-O-methyltransferase[J].Biochim Biophys Acta,1995,1251:1-10.
[5]Tenhunen J,Ulmanen I.Production of rat soluble and membrane-bound catechol O-methyltransferase forms from bifunctional m RNAs[J].Biochem J,1993,296(Pt 3):595-600.
[6]Tenhunen J,Salminen M,Lundstrom K,et al.Genomic organization of the human catechol O-methyltransferase gene and its expression from two distinct promoters[J].Eur J Biochem,1994,223:1049-1059.
[7]Guldberg HC,Marsden CA.Catechol-O-methyl transferase:pharmacological aspects and physiological role[J].Pharmacol Rev,1975,27:135-206.
[8]Roth JA.Membrane-bound catechol-O-methyltransferase:a reevaluation of its role in the O-methylation of the catecholamine neurotransmitters[J].Rev Physiol Biochem Pharmacol,1992,120:1-29.
[9]Ellingson T,Duddempudi S,Greenberg BD,et al.Determination of differential activities of soluble and membrane-bound catechol-O-methyltransferase in tissues and erythrocytes[J].J Chromatogr B Biomed Sci Appl,1999,729:347-353.
[10]Soares-da-Silva P,Fernandes MH,Pinto-do OP.Cell inward transport of L-DOPA and 3-O-methyl-L-DOPA in rat renal tubules[J].Br J Pharmacol,1994,112:611-615.
[11]Hansell P,Odlind C,Mannisto PT.Different renal effects of two inhibitors of catechol-O-methylation in the rat:entacapone and CGP 28014[J].Acta Physiol Scand,1998,162:489-494.
[12]Bidart JM,Motte P,Assicot M,et al.Catechol-O-methyltransferase activity and aminergic binding sites distribution in human peripheral blood lymphocyte subpopulations[J].Clin Immunol Immunopathol,1983,26:1-9.
[13]Tunbridge EM,Harrison PJ,Weinberger DR.Catechol-Omethyltransferase,cognition,and psychosis:Val158Met and beyond[J].Biol Psychiatry,2006,60:141-151.
[14]Karhunen T,Tilgmann C,Ulmanen I,et al.Distribution of catechol-O-methyltransferase enzyme in rat tissues[J].J Histochem Cytochem,1994,42:1079-1090.
[15]Mannisto PT,Ulmanen I,Lundstrom K,et al.Characteristics of catechol O-methyl-transferase(COMT)and properties of selective COMT inhibitors[J].Prog Drug Res,1992,39:291-350.
[16]Lotta T,Vidgren J,Tilgmann C,et al.Kinetics of human soluble and membrane-bound catechol O-methyltransferase:a revised mechanism and description of the thermolabile variant of the enzyme[J].Biochemistry,1995,34:4202-4210.
[17]Kiss LE,Soares-da-Silva P.Medicinal chemistry of catechol O-methyltransferase(COMT)inhibitors and their therapeutic utility[J].J Med Chem,2014,57:8692-8717.
[18]Ehler A,Benz J,Schlatter D,et al.Mapping the conformational space accessible to catechol-O-methyltransferase[J].Acta Crystallogr D Biol Crystallogr,2014,70:2163-2174.
[19]Saito S,Iida A,Sekine A,et al.Identification of 197 genetic variations in six human methyltranferase genes in the Japanese population[J].J Hum Genet,2001,46:529-537.
[20]Ji J,Tsuk S,Salapatek AM,et al.The 25-k Da synaptosomeassociated protein(SNAP-25)binds and inhibits delayed rectifier potassium channels in secretory cells[J].J Biol Chem,2002,277:20195-20204.
[21]Ball P,Knuppen R.Catecholoestrogens(2-and 4-hydroxyoestrogens):chemistry,biogenesis,metabolism,occurrence and physiological significance[J].Acta Endocrinol Suppl(Copenh),1980,232:1-127.
[22]Mannisto PT,Kaakkola S.Catechol-O-methyltransferase(COMT):biochemistry,molecular biology,pharmacology,and clinical efficacy of the new selective COMT inhibitors[J].Pharmacol Rev,1999,51:593-628.
[23]Lee E,Cho S,Kim K,et al.An integrated approach to infer causal associations among gene expression,genotype variation,and disease[J].Genomics,2009,94:269-277.
[24]Drew LJ,Crabtree GW,Markx S,et al.The 22q11.2microdeletion:fifteen years of insights into the genetic and neural complexity of psychiatric disorders[J].Int J Dev Neurosci,2011,29:259-281.
[25]Yavich L,Forsberg MM,Karayiorgou M,et al.Site-specific role of catechol-O-methyltransferase in dopamine overflow within prefrontal cortex and dorsal striatum[J].J Neurosci,2007,27:10196-10209.
[26]Dickinson D,Elvevag B.Genes,cognition and brain through a COMT lens[J].Neuroscience,2009,164:72-87.
[27]Meyer-Lindenberg A,Weinberger DR.Intermediate phenoltypes and genetic mechanisms of psychiatric disorders[J].Nat Rev Neurosci,2006,7:818-827.
[28]Qin X,Peng Q,Qin A,et al.Association of COMT Val158Met polymorphism and breast cancer risk:an updated meta-analysis[J].Diagn Pathol,2012,7:136.
[29]Cavalieri EL,Rogan EG.Unbalanced metabolism of endogenous estrogens in the etiology and prevention of human cancer[J].J Steroid Biochem Mol Biol,2011,125:169-180.
[30]Serretti A,Olgiati P.Catechol-O-methyltransferase and Alzheimer’s disease:a review of biological and genetic findings[J].CNS Neurol Disord Drug Targets,2012,11:299-305.
[31]Birks J.Cholinesterase inhibitors for Alzheimer’s disease[J].Cochrane Database Syst Rev,2006,25:CD005593.
[32]Raina P,Santaguida P,Ismaila A,et al.Effectiveness of cholinesterase inhibitors and memantine for treating dementia:evidence review for a clinical practice guideline[J].Ann Intern Med,2008,148:379-397.
[33]Perez-Madrinan G,Cook SE,Saxton JA,et al.Alzheimer disease with psychosis:excess cognitive impairment is restricted to the misidentification subtype[J].Am J Geriatr Psychiatry,2004,12:449-456.
[34]Ballard C,Creese B,Corbett A,et al.Atypical antipsychotics for the treatment of behavioral and psychological symptoms in dementia,with a particular focus on longer term outcomes and mortality[J].Expert Opin Drug Saf,2011,10:35-43.
[35]Pritchard AL,Pritchard CW,Bentham P,et al.Investigation of the role of the dopamine transporter in susceptibility to behavioural and psychological symptoms of patients with probable Alzheimer’s disease[J].Dement Geriatr Cogn Disord,2008,26:257-260.
[36]Seeman P,Caruso C,Lasaga M.Memantine agonist action at dopamine D2 High receptors[J].Synapse,2008,62:149-153.
[37]Giustizieri M,Cucchiaroni ML,Guatteo E,et al.Memantine inhibits ATP-dependent K+conductances in dopamine neurons of the rat substantia nigra pars compacta[J].J Pharmacol Exp Ther,2007,322:721-729.
[38]Worda C,Sator MO,Schneeberger C,et al.Influence of the catechol-O-methyltransferase(COMT)codon 158 polymorphism on estrogen levels in women[J].Hum Reprod,2003,18:262-266.
[39]Morinaga A,Hirohata M,Ono K,et al.Estrogen has antiamyloidogenic effects on Alzheimer’sβ-amyloid fibrils in vitro[J].Biochem Biophys Res Commun,2007,359:697-702.
[40]Liang K,Yang L,Yin C,et al.Estrogen stimulates degradation ofβ-amyloid peptide by up-regulating neprilysin[J].J Biol Chem,2010,285:935-942.
[41]Porrello E,Monti MC,Sinforiani E,et al.Estrogen receptorαand APOE 4 polymorphisms interact to increase risk for sporadic AD in Italian females[J].Eur J Neurol,2006,13:639-644.
[42]Craig MC,Murphy DG.Estrogen therapy and Alzheimer’s dementia[J].Ann N Y Acad Sci,2010,1205:245-253.
[43]Mc Caddon A,Davies G,Hudson P,et al.Total serum homocysteine in senile dementia of Alzheimer type[J].Int J Geriatr Psychiatry,1998,13:235-239.
[44]Chen CS,Chou MC,Yeh YC,et al.Plasma homocysteine levels and major depressive disorders in Alzheimer disease[J].Am J Geriatr Psychiatry,2010,18:1045-1048.
[45]Tunbridge EM,Harrison PJ,Warden DR,et al.Polymorphisms in the catechol-O-methyltransferase(COMT)gene influence plasma total homocysteine levels[J].Am J Med Genet B Neuropsychiatr Genet,2008,147B:996-999.
[46]de Lau LM,Breteler MM.Epidemiology of Parkinson’s disease[J].Lancet Neurol,2006,5:525-535.
[47]Gibb WR,Lees AJ.The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson’s disease[J].J Neurol Neurosurg Psychiatry,1988,51:745-752.
[48]Foltynie T,Goldberg TE,Lewis SG,et al.Planning ability in Parkinson’s disease is influenced by the COMT val158met polymorphism[J].Mov Disord,2004,19:885-891.
[49]Cheshire P,Bertram K,Ling H,et al.Influence of single nucleotide polymorphisms in COMT,MAO-A and BDNF genes on dyskinesias and levodopa use in Parkinson’s disease[J].Neurodegener Dis,2014,13:24-28.
[50]Wang Y,Yang X.Association of catechol-O-methyltransferase polymorphism(Val108/158Met)with Parkinson’s disease:a meta-analysis[J].J Mot Behav,2012,44:365-372.
[51]Maraganore DM,Lesnick TG,Elbaz A,et al.UCHL1 is a Parkinson’s disease susceptibility gene[J].Ann Neurol,2004,55:512-521.
[52]Lesage S,Brice A.Parkinson’s disease:from monogenic forms to genetic susceptibility factors[J].Hum Mol Genet,2009,18:R48-59.
[53]Connolly BS,Lang AE.Pharmacological treatment of Parkinson disease:a review[J].JAMA,2014,311:1670-1683.
[54]Kambur O,Mannisto PT.Catechol-O-methyltransferase and pain[J].Int Rev Neurobiol,2010,95:227-279.
[55]Kambur O,Mannisto PT,Viljakka K,et al.Stress-induced analgesia and morphine responses are changed in catecholO-methyltransferase-deficient male mice[J].Basic Clin Pharmacol Toxicol,2008,103:367-373.
[56]Davis WM,Hatoum NS,Khalsa JH.Toxic interaction between narcotic analgesics and inhibitors of catechol-Omethyltransferase[J].Toxicology,1979,14:217-227.
[57]Kambur O,Talka R,Ansah OB,et al.Inhibitors of catechol-Omethyltransferase sensitize mice to pain[J].Br J Pharmacol,2010,161:1553-1565.
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