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[3] [4] In some plant families (of the order Caryophyllales), l-DOPA is the central precursor of a biosynthetic pathway that produces a class of pigments called betalains. [5] l-DOPA can be manufactured and in its pure form is sold as a drug with the INN Tooltip International Nonproprietary Name levodopa. Trade names include Sinemet, Pharmacopa ...
Tyrosine hydroxylase or tyrosine 3-monooxygenase is the enzyme responsible for catalyzing the conversion of the amino acid L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA). [5] [6] It does so using molecular oxygen (O 2), as well as iron (Fe 2+) and tetrahydrobiopterin as cofactors.
Levodopa crosses the protective blood–brain barrier, whereas dopamine itself cannot. [3] [4] Thus, levodopa is used to increase dopamine concentrations in the treatment of Parkinson's disease, Parkinsonism, dopamine-responsive dystonia and Parkinson-plus syndrome. The therapeutic efficacy is different for different kinds of symptoms.
Levodopa (L-DOPA), a prodrug of dopamine which is used to treat Parkinson's disease and certain other conditions. A neurotransmitter prodrug, or neurotransmitter precursor, is a drug that acts as a prodrug of a neurotransmitter. A variety of neurotransmitter prodrugs have been developed and used in medicine.
It was named dopamine because it is a monoamine whose precursor in the Barger-Ewens synthesis is 3,4-dihydroxyphenylalanine (levodopa or L-DOPA). Dopamine's function as a neurotransmitter was first recognized in 1958 by Arvid Carlsson and Nils-Åke Hillarp at the Laboratory for Chemical Pharmacology of the National Heart Institute of Sweden. [155]
Aromatic L-amino acid decarboxylase is active as a homodimer.Before addition of the pyridoxal phosphate cofactor, the apoenzyme exists in an open conformation. Upon cofactor binding, a large structural transformation occurs as the subunits pull closer and close the active site.
Levodopa is a precursor to the neurotransmitter dopamine, which is administered to increase its levels in the central nervous system.However, most levodopa is decarboxylated to dopamine before it reaches the brain, and since dopamine is unable to cross the blood–brain barrier, this translates to little therapeutic gain with strong peripheral side effects.
Peripherally selective DDCIs incapable of crossing the protective blood–brain barrier (BBB) are used in augmentation of L-DOPA (levodopa) in the treatment of Parkinson's disease (PD) to block the conversion of L-DOPA into dopamine outside the brain, for the purpose of reducing adverse side effects. [3]