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Human DOPA Decarboxylase: Catalysis and Involvement in Pharmacological Treatments for Parkinson’s Disease and Aromatic Amino Acid Decarboxylase Deficiency
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Mariarita Bertoldi, Giada Rossignoli
The current therapy for PD is a combination of l-DOPA, that can cross the blood-brain barrier and reach neuronal DDC to increase dopamine content, with a peripheral inhibitor in order to modulate activity of peripheral DDC and allow a greater l-DOPA content to reach the brain (Singh et al., 2007; Kalinderi et al., 2011). The inhibitors commonly used contain a hydrazino group instead of an amino group that blocks the coenzyme in an inert hydrazone structure (Montioli et al., 2016). CarbiDOPA (L - α-methyl-α-hydrazino-2,3,4-trihydroxyphenylpropionic acid; MK485) patented by Merck in 1962, does not undergo degradation in vivo, while benserazide (N-(D,L-seryl)-N’-2,3,4-trihydroxybenzylhydrazine; Ro-4-4602), available in Europe since 1975, is cleaved into serine and 2,3,4-trihydroxybenzylhydrazine before reaching the blood-brain barrier (Schwartz and Brandt, 1978). Both carbiDOPA and benserazide are powerful irreversible inhibitors, while the precursor benserazide is a poor inhibitor with a Kļ = 0.3 mM (Borri-Voltattorni et al., 1977a; Borri-Voltattorni et al., 1977b; Borri Voltattorni et al., 1981). The main problem in the use of these inhibitors is that the hydrazine group is highly reactive towards all carbonyl groups and thus cannot discriminate among PLP enzymes (McCormick and Snell, 1959). The hydrazino compounds can interfere with tryptophan metabolism by interacting with kynureninase and kynurenine aminotransferase resulting in a decreased synthesis of nicotinamide (Bender and Smith, 1978). These alterations of the metabolic pathways of other amino acids could result in many adverse effects caused by the combination of l-DOPA with one of these peripheral inhibitors such as nausea, hypotension, arrhytmias, gastrointestinal bleeding and serious psychiatric symptoms (Rinne and Molsa, 1979).
Application of Microbial Enzymes in Industry and Antibiotic Production
Published in Pankaj Bhatt, Industrial Applications of Microbial Enzymes, 2023
Rishendra Kumar, Lokesh Tripathi, Pankaj Bhatt
L-dihydroxy phenylalanine (L-DOPA), a precursor for dopamine production, is a potential drug used to treat Parkinson’s disease and also to control the myocardium neurogenic injury. L-DOPA is produced by tyrosinase (Ikram-ul-Haq et al., 2002; Zaidi et al., 2014). The β-lactam antibiotics like penicillins and cephalosporins are largely produced in pharmaceutical companies with the help of enzymes (Volpato, 2010).
Production of Amino Acids by Fermentation
Published in Nduka Okafor, Benedict C. Okeke, Modern Industrial Microbiology and Biotechnology, 2017
Nduka Okafor, Benedict C. Okeke
In addition derivatives of amino acids are widely used in medicine as discussed below. Methyldopa (L-methy1-3, 4 dihydroxy-phenylalanine) is widely used as an anti- hypertensive with relatively few side effects. Dopa is used in treating Parkinson’s disease.
Kinetic modeling and statistical optimization of submerged production of anti-Parkinson’s prodrug L-DOPA by Pseudomonas fluorescens
Published in Preparative Biochemistry & Biotechnology, 2022
Ananya Naha, Santosh Kumar Jha, Hare Ram Singh, Muthu Kumar Sampath
Levodopa is an amino acid and a precursor of dopamine. It can easily cross the blood-brain barrier and convert to dopamine by Dopa Carboxylase by a single enzymatic step, thus increasing the store of dopamine in the brain. Unlike dopamine, L-DOPA can be taken orally or intravenously. It is rapidly taken up by dopaminergic neurons and converted to dopamine.[4] The conversion of L-DOPA to dopamine mainly occurs in the periphery as well as in Central Nervous System (CNS) thus facilitating the reuptake of dopamine by the dopamine transporter (DAT) and vesicular monoamine transporter (VMAT). DAT helps to transport dopamine from extracellular to intracellular space, and VMAT reloads dopamine into the vesi hcles. The whole process is energy-dependent and uses Na-K ions for ATP hydrolysis to create a concentration gradient of ions across the presynaptic membrane. This drive opens the transporter and cotransport Na and Cl ions and dopamine from the synaptic cleft. The released K ions in the synaptic cleft help in the equilibration of the ionic gradient across the presynaptic membrane. Metabolism of dopamine by monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) is one of the effective mechanisms for dopamine inactivation. This includes several pathways like oxidative deamination by MAO, conjugation by glucuronidase or sulfotransferases, and O-methylation by COMT. MAO acts intracellularly and is located at the external membrane of mitochondria, whereas COMT acts extracellularly and is located within the external cell membrane.[5]
Parkinson’s disease development prediction by c-granule computing compared to different AI methods
Published in Journal of Information and Telecommunication, 2020
Andrzej W. Przybyszewski, Albert Śledzianowski
We have tested two groups of PD patients: the first group (G1) of 23 patients was measured three times every half of the year (visits were numbered as V1, V2, V3) and the second group (G2) had more advanced 24 patients and were a reference model of disease progression in the first group. Both groups of patients were only on medication. The major medication in this group was l-Dopa that increases the concentration of the transmitter dopamine in the brain which is lacking in Parkinson’s patients. In most cases, PD starts with ND in substantia nigra that is responsible for the release of dopamine.