The first and most obvious way is through the inhibition of MAO-B. More than 80 percent of the dopamine in the human brain is in the basal ganglia. MAO-B in the basal ganglia is almost completely inhibited by taking 10 mg a day of deprenyl, resulting in a 40 to 70 percent increase in dopamine. MAO-B inhibition reduces degradation of phenylethylamine even more effectively than it inhibits dopamine degradation. Phenylethylamine stimulates release of dopamine and serotonin, besides acting as a direct stimulant on dopamine receptors. The breakdown products of dopamine resulting from MAO-B degradation are hydrogen peroxide, ammonia and an aldehyde.
Aldehydes are highly reactive compounds that can modify proteins.
Hydrogen peroxide in the presence of ferrous iron ions can lead to hydroxyl radicals, the most toxic of all free radicals. Joseph Knoll has contended that it is this effect of deprenyl, rather than MAO-B inhibition, that results in life span extension. Thus, inhibition of MAO-B metabolism of dopamine seems unlikely to be the mechanism by which deprenyl extends a rat's life span. The dose of deprenyl required to cause the production of antioxidant enzymes is highly dependent upon the strain, age, sex and species of animal. The equivalent of 75 mg a day for a 170-pound person produced optimal superoxide dismutase in old C57BL male mice and female beagles.