Anti-MAO-B: Rabbit Monoamine Oxidase B Antibody

There are two MAO isoenzymes, MAO-A and MAO-B, which differ by their substrate specificity and even more by inhibitor selectivity. The genes coding for MAO-A and MAO-B are both located on the short arm of the X chromosome. Comparison of the deduced amino-acid sequences showed that MAO-A and MAO-B have around 70% amino-acid sequence identity. The two genes MAOA and MAOB are arranged in a tail-to-tail orientation, and both span at least 60 kb, consist of 15 exons, and exhibit an identical exon-intron organization. The promoter regions share 60% sequence homology and both promoters consist of GC-rich regions. MAO-A is inhibited by low concentrations of clorgyline whereas MAO-B is irreversibly inhibited by low concentrations of deprenyl.² In humans, the highest concentrations of MAO-A are found at the organism’s barrier: gut, placenta, lungs and liver, corresponding to the enzyme’s ontogenetic detoxifying function. High concentrations of MAO-B are found in glial cells and blood platelets. Moreover, MAO-B is primarily found in the brain, accounting for 70%–80% of MAO in the brain. MAO-A preferentially deaminates bioamines of endogenous source such as 5-HT, epinephrine and NE, while MAO-B is the major metabolic step for changing active dopamine to its inactive catabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid. MAO-B preferentially degrades exogenous bioamines ingested in the diet such as phenylethylamine and benzylamine. Dopamine and tyramine are equally catabolized by both forms of MAO. These substrate specificities are relative, however, since, depending on conditions, all the above bioamines are substrates for both isoenzymes. End products of the MAO action on bioamines are aldehydes and H2O2 involved in oxidative processes. Aldehydes are either oxidized in 5-hydroxy indol acetic acid (5-HIAA) for 5-HT catabolism or reduced in 3,4-dihydroxyphenylglycol (DHPG) for NE catabolism. The formation of 5-HIAA from 5-HT via MAO is accompanied by the generation of ROS which participate in smooth muscle cell proliferation, hypoxia and respiratory distress and cancer growth. Various MAO-B inhibitors are used for the treatment of Parkinson’s disease. The antiparkinsonian effect of MAO-B inhibitors is primarily attributed to decrease the rate of turnover of striatal dopamine and prolong the duration of action of both endogenously and exogenously derived dopamine.³