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Cardiac Sympathetic Neuroimaging
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
From kinetic modeling one can predict that, all other things being the same, translocation of vesicles to the membrane surface and an increased rate of exocytosis will produce a pattern of decreased peak 123I-MIBG-derived radioactivity and more rapid loss of the radioactivity. Another mechanism may be high enough circulating catecholamine concentrations to compete with 123I-MIBG for neuronal uptake via the cell membrane norepinephrine transporter (25). High local norepinephrine concentrations at uptake-1 sites in the hearts of patients with high cardiac sympathetic nerve traffic might also compete for neuronal uptake of 123I-MIBG and promote accelerated loss of radioactivity by attenuating reuptake. Moreover, general intraneuronal pathophysiologic changes, such as cellular hypoxia or acidosis, would be expected to decrease the efficiency of the vesicular monoamine transporter or cell membrane norepinephrine transporter, activities of which depend on energy-requiring processes.
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]