The following points highlight the four main processes of Decarboxylation. The processes are: 1. Tyramine 2. Tryptamine 3. Histamine 4. GABA (γ-aminobutyric acid).
Decarboxylation Process # 1. Tyramine:
i. Tyramine is formed from tyrosine by tyrosine decarboxylation causing elevation of blood pressure.
ii. This occurs in the gut by bacterial action.
iii. The reaction takes place also in the kidney being favoured by oxygen deficiency.
iv. The tissue deaminates tyrosine in presence of sufficient oxygen.
Decarboxylation Process # 2. Tryptamine:
i. Tryptamine is formed from the amino acid tryptophan by the enzyme tryptophan decarboxylase present in mammalian kidney, liver and bacteria of gut involving (B6-PO4) as a coenzyme.
ii. Derivative of 5-OH tryptamine is serotonin a tissue hormone.
iii. It also increases blood pressure.
Decarboxylation Process # 3. Histamine:
i. The enzyme histidine decarboxylase, in presence of the coenzyme (B6-PO4), catalyze the conversion of histidine to histamine.
ii. This is produced by gastric mucosa cells and histaminergic neurons of the central nervous system.
iii. This is produced in the gut by bacterial decarboxylation of histidine.
iv. Basophils, another principal source of histamine, in the circulating cells.
v. In the hypothalamus, it acts as a neurotransmitter.
vi. It serves as an anaphylactic and inflammatory agent in response to antigen.
vii. Effects of released histamine are mediated through H1 and H2 receptors.
viii. It is formed in injured tissues. The liberation of histamine excessively is related to traumatic shock.
ix. Its elevated level depresses blood pressure and large doses cause extreme vascular collapse.
x. The increased plasma level of histamine is found in patients with antigen-induced bronchial asthma.
xi. The anaphylactic reactions of histamine is mixed by promethazine and mepyramine which block H1 receptors and cimetidine, the blocker of H2 receptors, reduce the gastric acidity in peptic ulcer patients.
xii. In the kidneys, the enzyme histaminase oxidatively deaminates histamine to β-imidazole acetaldehyde which is further oxidized in the liver by aldehyde oxidase to form β-imidazole acetic acid which is excreted in urine—being conjugated with ribose.
Decarboxylation Process # 4. GABA (γ-aminobutyric acid):
i. GABA is formed principally in CN system in grey matter from glutamate by the catalytic activity of the enzyme glutamate decarboxylase with (B6-PO4) as coenzyme.
ii. It acts as a normal regulator of neuronal activity being active as an inhibitor.
iii. It is released at the axon terminals of neurons in grey matter and acts as inhibitory neurotransmitter by accelerating K+ permeability of post synaptic membranes.
iv. The vitamin Pyridoxine (vit. B6) deficiency forms GABA in less amount leading to neuronal hyper-excitability and convulsions.
v. GABA is metabolised to form succinic semi-aldehyde by deamination in presence of (B6-PO4) as coenzyme and the ammonia removed is trans-aminated to α-ketoglutarate forming more glutamate.
