Дисертації з теми "Methionase enzyme"
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Lou, Xiao. "Biochemical and structural studies of human methionine synthase reductase." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/biochemical-and-structural-studies-of-human-methionine-synthase-reductase(822952fc-8bef-4a30-9221-7fb154638193).html.
Повний текст джерелаDhouib, Rabeb, Dk Seti Maimonah Pg Othman, Victor Lin, Xuanjie J. Lai, Hewa G. S. Wijesinghe, Ama-Tawiah Essilfie, Amanda Davis, et al. "A Novel, Molybdenum-Containing Methionine Sulfoxide Reductase Supports Survival of Haemophilus influenzae in an In vivo Model of Infection." FRONTIERS MEDIA SA, 2016. http://hdl.handle.net/10150/622464.
Повний текст джерелаSampson, Peter B. "Synthesis of potential inhibitors targeting enzymes involved in methionine biochemistry." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape3/PQDD_0018/NQ53511.pdf.
Повний текст джерелаHuber, Tyler D. "TOWARD AN ENZYME-COUPLED, BIOORTHOGONAL PLATFORM FOR METHYLTRANSFERASES: PROBING THE SPECIFICITY OF METHIONINE ADENOSYLTRANSFERASES." UKnowledge, 2019. https://uknowledge.uky.edu/pharmacy_etds/106.
Повний текст джерелаVelichkova, Polina. "Modeling of methyl transfer reactions in S-Adenosyl-L-Methionine dependent enzymes." Licentiate thesis, Stockholm, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-3910.
Повний текст джерелаGagliano, Elisa. "A Bioinformatics Approach to Identifying Radical SAM (S-Adenosyl-L-Methionine) Enzymes." Thesis, Virginia Tech, 2020. http://hdl.handle.net/10919/98736.
Повний текст джерелаMaster of Science in Life Sciences
Radical SAM enzymes are ancient, essential enzymes that perform chemical reactions in virtually all living organisms. We do know that they are involved in producing antibiotics, human health, and generating greenhouse gases. We also know that there are many radical SAM enzymes whose functions remain a mystery. There have been great leaps forward in the amount of enzyme sequences that are available in public databases, but experiments to investigate what chemical reactions enzymes perform take a great deal of time. The experiments are especially difficult for radical SAM enzymes because the oxygen we breathe can break the enzymes down in a laboratory. In our work, we utilize computational techniques to identify possible radical SAM enzymes and predict what reactions they might catalyze. Because these enzymes are vulnerable to oxygen in laboratory environments, we also explore whether organisms that breathe oxygen have fewer of these enzymes than organisms that perform anaerobic respiration instead. We found that does seem to be the case in microbes like bacteria and archaea, but the results were not as consistent for eukaryotes. We then chose radical SAM enzymes we had identified from both an aerobic eukaryote (Entamoeba histolytica) and a eukaryote capable of producing oxygen (Gossypium barbadense), and predicted the reactions they catalyze. This work sets the stage for the functional characterization of these essential yet elusive enzymes in future laboratory experiments.
Yanamadala, Srinivasa Rao. "Molecular cloning and characterization of regulatory enzymes in threonine biosynthetic pathway from soybean." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/4932.
Повний текст джерелаThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on May 12, 2009) Includes bibliographical references.
Johnson, Bernadette. "Fluorinated #alpha#-amino acid analogues of L-methionine and related compounds for use as potential enzyme inhibitors." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264261.
Повний текст джерелаYoung, Anthony Peter, and Anthony Peter Young. "Characterization of 4-demethylwyosine Synthase, a Radical S-adenosyl-l-methionine Enzyme Involved in the Modification of tRNA." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/621437.
Повний текст джерелаWang, Xiao Suo. "A novel ELISA to detect methionine sulfoxide-containing apolipoprotein A-I." Connect to full text, 2009. http://hdl.handle.net/2123/5423.
Повний текст джерелаSubmitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Pathology, Faculty of Medicine. Title from title screen (viewed Sept. 30, 2009) Includes bibliography. Also available in print form.
Grell, Tsehai A. J. (Tsehai Ariane Julien). "Structural studies of S-adenosyl-L-methionine radical enzymes involved in tRNA and natural product biosynthesis." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/118265.
Повний текст джерелаCataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Members of the S-adenosyl-L-methionine (AdoMet) radical enzyme superfamily catalyze a myriad of diverse and challenging biotransformations using a [4Fe-4S] cluster and a molecule of AdoMet to initiate radical. In this thesis, we used a combination of crystallographic and biochemical methods to identify the use of covalent catalysis and polar reactions in two AdoMet radical enzymes that catalyze the key steps in the biosynthesis of the tRNA modified bases wybutosine and queuosine. TYWI catalyzes the formation of the characteristic imidazopurine ring of wybutosine through a disputed mechanism. Here, we have garnered support for one of the proposed mechanisms, through the identification and characterization of a Schiff base between a catalytically essential lysine residue and the substrate pyruvate. The ability of TYWI to form and possibly use a Schiff base presents the first instance of a covalent catalysis in the mechanism of an AdoMet radical enzyme. In an attempt to obtain a snapshot of the active site of the queuosine biosynthetic enzyme, QueE, with AdoMet and a substrate analog, 6-carboxypterin (6-CP), we uncovered a covalent adduct between AdoMet and 6-CP. Further investigation of the mechanism by which this adduct was formed revealed a polar mechanism instead of a radical one. This result highlights the ability for AdoMet radical enzymes to use the same active site for two different reactions, polar and/or radical reactions. The unifying characteristics of this superfamily include the canonical CX₃CX[phi]C cluster-binding motif and a partial ([beta]/[alpha]X) 6 triose isomerase phosphate (TIM) barrel. Work in this thesis presents the structural characterization of a third QueE ortholog from Escherichia coli. Together, these three QueE orthologs revealed different variations in the core barrel architecture, which may influence binding of the biological reductant Flavodoxin. This variance in the core AdoMet radical fold emphasizes the structural diversity of this superfamily. On the other hand, we see conservation of an overall three-domain architecture for the maturation of ribosomally synthesized and post-translationally modified natural products, underlining the importance of this architecture for catalysis.
by Tsehai A.J. Grell.
Ph. D. in Biological Chemistry
Suh-Lailam, Brenda Bienka. "Development of Novel Methods and their Utilization in the Analysis of the Effect of the N-terminus of Human Protein Arginine Methyltransferase 1 Variant 1 on Enzymatic Activity, Protein-protein Interactions, and Substrate Specificity." DigitalCommons@USU, 2010. https://digitalcommons.usu.edu/etd/863.
Повний текст джерелаBarp, Jaqueline. "Avaliação do dano oxidativo e função cardiovascular em diferentes modelos de hiperhomocisteinemia : papel protetor do folato e do estrogênio." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2007. http://hdl.handle.net/10183/11795.
Повний текст джерелаIt is known that high concentrations of homocysteine (Hcy) are associated with the increase of risk of cardiovascular disease and of cellular damage caused by the formation of reactive oxygen species (ROS). It is also known that the estrogen acts as a non enzymatic antioxidant involved in cardiovascular protection. In this work we evaluated the effect of homocystinuria on myocardial oxidative stress parameters, and the effect of hyperhomocysteinemia (HHcy) on the same parameters and also on hemodynamics in rats with and without estrogen. Four experiments were performed. In experiment number one, sixteen animals were divided in 2 groups (n=8/group): control and Hcy. These animals received chronic treatment from the 6th to the 28th day of life with increasing doses of Hcy and were killed one hour after the last dose. In the second experiment, thirty rats were divided into four groups: Saline (n=8); Folate (n=6); Hcy (n=9) and Folate+Hcy (n=7).These animals had received folic acid and/or Hcy from the 6th to the 28th day of life and had been killed with 80 days of life. In the third experiment, fourty eight animals were divided in 6 groups (n=8/group): NAIVE; NAIVE+Hcy; Sham; Sham+Hcy; castrated and castrated+Hcy. These animals were castrated in the 50th day of life and, after one week, they received an acute treatment with Hcy for 72 hours at each eight hours and were killed one hour after the last dose. In the fourth experiment, thirty two animals were divided into four groups (n=8/group): control, castrated, methionine and castrated+methionine. These animals had been castrated in the 70th day of life, and received methionine in drinking water for 30 days and were killed at the end of treatment. In the homocystinuria model (experiment number one), there were no signs of alterations in lipid peroxidation (LPO) in 28 day rats. However, antioxidant enzyme activities of SOD and GST were increased in Hcy group. As this is a chronic treatment, probably these enzymes are increased to minimize the oxidative damage caused by Hcy. In the second experiment, the effect of the homocystinuria was evaluated in animals with 80 days. It was observed an increase in LPO in the animals that had received Hcy, but it returned to control values with folate administration. The reduction of LPO in the presence of folate confirms its capacity of minimize the damage caused by Hcy. We also observedreduction in the enzyme activities of GST and catalase in the animals receiving Hcy, which also returned to the control values with the administration of folate. It is possible that Hcy increases the hydrogen peroxide concnetration in the myocardium of these animals. From the results obtained, we can suggest that the levels of Hcy can be reduced with folate, since high doses of folate had significantly reduced the levels of oxidative stress caused by Hcy. In the acute model of HHcy (experiment number three), myocardial oxidative stress increased due to the administration of Hcy in the group without estrogen. This result has a positive correlation with mean arterial pressure (MAP), that is, the higher LPO, the higher MAP. This effect was not observed in groups with physiological estrogens levels. It is possible that these findings are related to the antioxidant protection offered by estrogen. Moreover, we observed a reduction in the activity of GST in the group castrated+Hcy, which can be contributing for the oxidative damage observed. In the HHcy model caused by the consumption of methionine (experiment number four), we observedThis result has a negative correlation with the nitric oxide metabolites (Nox) showing that the animals that had an increased ventricular diastolic pressure had presented lesser NO bioavailability. In this model we also observed an increase in the myocardial oxidative stress due to the administration of methionine in the group without estrogen. This result has a positive correlation with LVEDP, that is, the animals with enhanced LPO also presented high ventricular diastolic pressure, indicating a possible participation of oxidative stress in ventricular dysfunction. These animals also presented an increase in the activities of GST and GPx in group castrated+methionine, suggesting that chronic treatment with methionine leads to an adaptation of the enzymatic antioxidant system in the absence of the estrogen.
Lee, Bong Joo. "Effects of dietary level of indispensable amino acids and feeding strategies on growth and biochemical responses in Atlantic salmon Salmo salar L." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376967154.
Повний текст джерелаPunekar, Avinash S. "Ribosomal RNA Modification Enzymes : Structural and functional studies of two methyltransferases for 23S rRNA modification in Escherichia coli." Doctoral thesis, Uppsala universitet, Struktur- och molekylärbiologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-212394.
Повний текст джерелаRavanel, Stéphane. "Biosynthèse de la méthionine chez les plantes supérieures : étude biochimique et moléculaire des enzymes de la voie de transsulfuration." Université Joseph Fourier (Grenoble ; 1971-2015), 1995. http://www.theses.fr/1995GRE10238.
Повний текст джерелаLibiad, Marouane. "La free R Méthionine sulfoxyde réductase (fRMsr) de Neisseria meningitidis : Mécanisme, catalyse et spécificité structurale." Thesis, Université de Lorraine, 2012. http://www.theses.fr/2012LORR0335/document.
Повний текст джерелаMethionine sulfoxide reductases (Msr) catalyze the specific reduction of methionine sulfoxides (Met-O) into methionine (Met). They are involved in cell defences against oxidative stress and virulence of pathogenic bacteria of Neisseria genius. This family of enzymes consists of three classes, MsrA and MsrB, structurally-unrelated, Specific for the S and the R epimer of the sulfoxide function of the substrate, respectively. A third class, recently discovered and called fRMsr, selectively reduce the free form of the R epimer of the sulfoxide function. The fRMsr belongs to the family of GAF domains, they are usually involved in cell signaling, and fRMsr represent the first GAF domain to show enzymatic activity. The studies of the Neisseria meningitidis fRMsr have shown that: 1) The Neisseria meningitidis fRMsr have a identical catalytic mechanism to MsrA and MsrB with the formation of at least one intramolecular disulfide bond, Cys84-Cys118 reduced by thioredoxin (Trx) ; 2) The Cys118 is demonstrated to be the catalytic Cys on which a sulfenic acid is formed ; 3) The Reductase step is the rate determining step of the mechanism leading to the formation of the disulfide bond Cys84-Cys118. The combination of the biochemical and kinetics data, and the examination of the 3D structure of the N. meningitidis fRMsr in complex with its substrate shown: 1) an oxyanion hole involved in the accommodation of the carboxylate group ; 2) the carboxylate group of the Asp143 residue involved in the catalysis of step reductase, and 3) The Glu125 residue involved in the recognition and/or positioning of the Met-O probably by the stabilization of the NH3+; 4) the Asp141 residue involved in the positioning of Asp143 and Glu125 residues ; 5) the indole ring of the Trp62 residue involved in stabilizing of the epsilon-methyl group
BERTHALON, ETIENNE. "Regulation de la voie de biosynthese de l'ethylene dans les cellules de tabac en culture sous l'effet d'eliciteurs fongiques." Toulouse 3, 1986. http://www.theses.fr/1986TOU30236.
Повний текст джерелаMarreiros, Maria Inês Moreira Oliveira Leite. "Characterization of Plasmodium methionine metabolism key enzyme." Master's thesis, 2016. http://hdl.handle.net/10451/25946.
Повний текст джерелаMalaria is a disease caused by protozoan parasites of the genus Plasmodium that are transmitted to humans by infected female Anopheles mosquitoes. Despite countless efforts toward eradication malaria still remains one of the most prevalent infectious diseases, constituting a major public health concern. The available antimalarial drugs are insufficient to control and eradicate malaria, mostly due to the emergence of drug-resistant parasites. Thus, the development of novel intervention strategies is critical to achieve eradication. As an obligatory intracellular pathogen, Plasmodium establishes close interactions with its host that are crucial to ensure parasite development and survival, one of such is the methionine metabolism. Methionine is an essential amino acid and, as for most living organisms, Plasmodium lacks the ability to synthesize methionine de novo. During the blood-stage of infection Plasmodium obtains methionine mainly through haemoglobin digestion. However, how Plasmodium obtains methionine during the liver-stage and how the parasite modulates the host cells in order to scavenge this essential amino acid is still unknown. The first step of methionine cycle is the synthesis of S-adenosylmethionine (SAMe) through a reaction catalyzed by the enzyme SAMe synthetase (SAMS). SAMe is a key metabolite in the methionine metabolism being the main biological donor of methyl groups for transmethylation reactions. SAMe is also a key intermediate in the transsulfuration pathway generating homocysteine (Hcy) which is metabolized into glutathione (GSH), being the last step of this pathway catalysed by glutathione synthetase (GS). GSH is a powerful antioxidant that in Plasmodium acts as one of the primary lines of the defense against the damage caused by reactive oxygen species (ROS), ensuring parasite survival. In this work we have explored the role of Plasmodium enzymes responsible for SAMe and GSH synthesis throughout its life cycle and in particular during the liver-stage of infection. The liver is a particular organ in the metabolism of methionine, namely in SAMe-dependent transmethylation reactions and in glutathione synthesis and storage. Thus, we hypothesized that while replicating inside hepatocytes, Plasmodium relies on its host to ensure a sufficient supply of these crucial metabolites. The data obtained in this study suggest that: 1) Plasmodium does not rely on its own SAMS enzyme while developing inside hepatocytes; 2) that the inhibition of SAMS activity during the blood-stage of infection leads to a low parasitemia, preventing the onset of cerebral malaria and 3) the deletion of GS-encoding gene results in the arrest at the oocyst stage, preventing transmission between the mosquito vector and the mammalian host. A detailed knowledge of Plasmodium methionine pathway provides promising tools for the design and development of novel antimalarial drugs.
A malária é uma doença causada por parasitas protozoários pertencentes ao género Plasmodium que são transmitidos aos humanos por mosquitos fêmea do género Anopheles. Apesar dos inúmeros esforços realizados na tentativa de erradicar a malária esta permanece ainda uma das doenças parasíticas mais prevalentes, constituindo um problema de saúde público. Os anti-maláricos disponíveis são insuficientes no controlo e erradicação da malária, devido sobretudo ao aparecimento de parasitas resistentes. Além disso, o escasso conhecimento acerca da biologia do parasita bem como das interações que este estabelece com o hospedeiro constituem uma barreira na luta contra a malária. Assim, o desenvolvimento de novas estratégias de intervenção torna-se crucial para conseguir a erradicação. Plasmodium é um patogénio intracelular obrigatório e, como tal, as interações que estabelece com o seu hospedeiro são essenciais para garantir o seu desenvolvimento e sobrevivência, nomeadamente as que estabelece ao nível do metabolismo da metionina. A metionina é um aminoácido essencial pelo que, tal como na maioria dos organismos, Plasmodium não tem capacidade para a sintetizar de novo. Durante a fase sanguínea Plasmodium obtém metionina maioritariamente através da degradação de hemoglobina. Contudo, os mecanismos que Plasmodium utiliza para obter metionina durante a fase hepática, bem como para modular a célula hospedeira de modo a garantir um fornecimento suficiente deste aminoácido são ainda desconhecidos. O primeiro passo do ciclo da metionina consiste na síntese de S-adenosilmetionina (SAMe) numa reação catalisada pela enzima SAMe sintetase (SAMS). A SAMe é um metabolito essencial na via metabólica da metionina sendo o maior dador biológico de grupos metilo. A SAMe é ainda um importante intermediário na via da transsulfuração sendo convertida em homocisteína e subsequentemente metabolizada em glutationo, sendo o último passo desta via catalisado pela glutationo sintetase (GS). O glutationo é um antioxidante que em Plasmodium atua como uma das primeiras linhas de defesa contra espécies oxidativas. Neste trabalho explorámos o papel das enzimas de Plasmodium responsáveis pela síntese de SAMe e glutationo ao longo do seu ciclo de vida, com particular ênfase na fase hepática da infeção. O fígado tem um papel preponderante no metabolismo da metionina, nomeadamente nas reações de transmetilação dependentes de SAMe bem como na regulação da síntese e armazenamento do glutationo. Assim, a hipótese que propusemos testar é que enquanto replica no interior do hepatócito Plasmodium depende do hospedeiro para garantir a obtenção destes metabolitos essenciais. Os resultados obtidos neste estudo demonstram que: 1) durante o seu desenvolvimento no fígado Plasmodium não depende da atividade da sua enzima SAMS; 2) a inibição da atividade da enzima SAMS durante a fase sanguínea da infeção resulta numa redução da parasitémia, prevenindo o aparecimento de malária cerebral e ainda que; 3) a deleção do gene que codifica para a enzima GS inibe o desenvolvimento dos esporozoítos, bloqueando assim a transmissão entre o vetor e o hospedeiro mamífero. Assim, um conhecimento detalhado do metabolismo da metionina em Plasmodium fornece ferramentas promissoras para o desenvolvimento de novos anti-maláricos.
Chou, He Yen, and 周和諺. "Functional study of methionine salvage pathway enzyme DADI1 and the biological role of methionine salvage pathway in Drosophila." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/20944365295796751105.
Повний текст джерела長庚大學
生物醫學研究所
102
As an essential amino acid, methionine plays crucial roles in multiple cellular processes. Except from diet, methionine contents are controlled by several pathways, including the folate pathway, transmethylation pathway (Methyl cycle) and methionine salvage pathway (MTA cycle). The MTA cycle is highly conserved from prokaryote to eukaryote and is distributed to regenerate methionine. However, the role of MTA cycle in physiological function is still unclear. Here, we employed MTA cycle enzyme, Drosophila aci-reductone dioxygenase 1 (DADI1), to investigate MTA cycle function in vivo. Our data demonstrated DADI1 is involved in methionine metabolism by targeted metabolites analysis. A significant decrease of methionine contents in Dadi1 mutants were found, indicating that the MTA cycle and Methyl cycle may contribute equally to regulating the level of methionine in Drosophila ovaries. Moreover, S-adenosylmethionine (SAM) and Methionine sulfoxide were also dramatic reduced, indicating that methionine related metabolites may be directly altered by MTA cycle. Furthermore, we link the MTA cycle to morphogenesis in Drosophila. The data showed that DADI1 was required for adhesion molecule Fasciclin III (FasIII) membrane expression in dorsal follicle cells and involved in dorsal appendage (DA) tubulogenesis. The defects in Dadi1 mutant cells were rescued by expressing wild-type DADI1 and human ADI1 but not ADI1 enzyme-dead mutant. Moreover, DADI1 showed genetic interaction with MTA cycle enzymes to participate in the regulation of FasIII membrane accumulation. Disrupting sam synthetase (sam-s) mimicked the effects of Dadi1 mutant in FasIII expression. Using targeted metabolites analysis, the levels of SAM were decreased substantially in sam-s mutant. In contrast, the levels of methionine increased in sam-s mutant. Supplying methionine recovered FasIII and DA defect in Dadi1 mutant but not in sam-s mutant egg chambers indicated SAM is key metabolite in regulation of FasIII expression. In addition, we revealed that SAM contents modulate the COPI mediated protein trafficking. Dadi1 and sam-s genetically interacted with COPI subunits to control FasIII expression. Knockdown COPI subunit, γCOP, by RNAi in follicle cells also caused a reduction in FasIII expression. An impairment of αCOPI signals were observed in Dadi1 mutant and sam-s mutant cells. Golgi morphology was significantly altered in Dadi1 mutant and sam-s mutant cells. Using density gradient fraction analysis, the distribution of αCOP was affected in Dadi1 mutant ovary. The protein methylation in Dadi1 mutant ovary was reduced, and a methylation inhibitor reduced FasIII expression. Together, our data demonstrate that the content of SAM may regulate membrane protein trafficking through the Golgi by controlling protein methylation, and the MTA cycle contributes to morphogenesis during development by modulating SAM contents.
Lu, Wei-Cheng. "Evolved enzymes for cancer therapeutics and orthogonal systems." 2013. http://hdl.handle.net/2152/23028.
Повний текст джерелаtext
Ubhi, Devinder Kaur. "Structural analysis and discovery of lead compounds for the fungal methionine synthase enzyme." Thesis, 2013. http://hdl.handle.net/2152/28686.
Повний текст джерелаtext
Paley, Olga M. "Engineering a novel human methionine degrading enzyme as a broadly effective cancer therapeutic." Thesis, 2014. http://hdl.handle.net/2152/31302.
Повний текст джерелаtext
Dawson, Karen. "The Catalytic Aspartic Acid Shows a Role in Substrate Positioning in 5-methylthioribose Kinase." Thesis, 2012. http://hdl.handle.net/1807/32571.
Повний текст джерелаRomero-Angulo, Hernán Mauricio. "On the role of the enzyme peptide methionine sulfoxide reductase in the response of Arabidopsis plants to oxidative stress." 2005. http://etda.libraries.psu.edu/theses/approved/WorldWideIndex/ETD-1035/index.html.
Повний текст джерелаWood, John M., Nick C. Gibbons, Elloof M. M. Abou, and Karin U. Schallreuter. "Hydrogen peroxide-mediated oxidative stress disrupts calcium binding on calmodulin: more evidence for oxidative stress in vitiligo." 2009. http://hdl.handle.net/10454/3001.
Повний текст джерелаPatients with acute vitiligo have low epidermal catalase expression/activities and accumulate 10 -3 M H 2O 2. One consequence of this severe oxidative stress is an altered calcium homeostasis in epidermal keratinocytes and melanocytes. Here, we show decreased epidermal calmodulin expression in acute vitiligo. Since 10 -3M H 2O 2 oxidises methionine and tryptophan residues in proteins, we examined calcium binding to calmodulin in the presence and absence of H 2O 2 utilising 45calcium. The results showed that all four calcium atoms exchanged per molecule of calmodulin. Since oxidised calmodulin looses its ability to activate calcium ATPase, enzyme activities were followed in full skin biopsies from lesional skin of patients with acute vitiligo (n = 6) and healthy controls (n = 6). The results yielded a 4-fold decrease of ATPase activities in the patients. Computer simulation of native and oxidised calmodulin confirmed the loss of all four calcium ions from their specific EF-hand domains. Taken together H 2O 2-mediated oxidation affects calcium binding in calmodulin leading to perturbed calcium homeostasis and perturbed L-phenylalanine-uptake in the epidermis of acute vitiligo.