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A family of pyridoxal phosphate-dependent enzymes involved in cellular nitrogen metabolism, amino acid metabolism, and liver gluconeogenesis. Alanine aminotransferase specifically and reversibly catalyzes the transfer of an amino group from L-alanine to alpha-ketoglutarate forming pyruvate and L-glutamate.
Indicadores
A family of pyridoxal phosphate-dependent enzymes involved in amino acid metabolism and in the urea and tricarboxylic acid cycles. Aspartate aminotransferase specifically and reversibly catalyzes the transfer of an amino group from L-aspartate to alpha-ketoglutarate forming oxaloacetate and L-glutamate.
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A non-essential alpha-amino acid and excitatory neurotransmitter. Glutamic acid can serve as a precursor for the synthesis of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA).
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A nonessential amino acid. Glutamine can donate the ammonia on its side chain to the formation of urea (for eventual excretion by the kidneys) and to purines (necessary for the synthesis of nucleic acids). Glutamic acid-to-glutamine conversion, in which an ammonia group is added to glutamic acid (catalyzed by glutamine synthase), is of central importance in the regulation of toxic levels of ammonia in the body. This agent is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and GABA) and is also an important source of energy for the nervous system. Glutamine may become a conditionally essential amino acid during certain catabolic states.
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A non-essential, non-polar, non-optical, glucogenic amino acid. Glycine, an inhibitory neurotransmitter in the CNS, triggers chloride ion influx via ionotropic receptors, thereby creating an inhibitory post-synaptic potential. In contrast, this agent also acts as a co-agonist, along with glutamate, facilitating an excitatory potential at the glutaminergic N-methyl-D-aspartic acid (NMDA) receptors. Glycine is an important component and precursor for many macromolecules in the cells.
Indicadores
A long-acting barbituric acid derivative with antipsychotic property. Phenobarbital binds to and activates the gamma-aminobutyric acid (GABA)-A receptor, thereby mimicking the inhibitory actions of GABA in the brain. The activation effects of the phenobarbital-receptor-ionophore complex include increased frequency of chloride channel openings, membrane hyperpolarization and ultimately synaptic inhibition and decreased neuronal excitability. In addition, this agent inhibits glutamate induced depolarization.