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Deamination occurs mainly in liver mitochondria, with the kidneys also contributing to ammonia handling and acid–base balance. In the principal oxidative pathway, glutamate dehydrogenase (GDH) converts glutamate to α-ketoglutarate and ammonia; its activity responds to cellular energy signals. For many amino acids, transamination first transfers amino groups to glutamate, which can then undergo oxidative deamination. Other routes include oxidative reactions involving amino acid oxidases, non-oxidative removal of ammonia, and hydrolytic deamination. Released ammonia is directed toward urea formation in the liver or renal excretion, while keto-acid products can enter pathways such as the TCA cycle. Understanding this coordination helps explain the metabolic and clinical importance of deamination.