The levels of norharman are high enough after smoking to affect monoamineoxidase B in platelets.

Epidemiological studies suggest that smoking reduces the risk for Parkinson's disease. It has been hypothesized that inhibition of monoamineoxidase contributes to this action. The present study examined the contribution of the beta-carbolines norharman, an inhibitor of monoamineoxidase B, and harman, an inhibitor of monoamineoxidase A, which are present in high concentrations in tobacco smoke to the protective action. Nineteen active smokers and five nonsmokers smoked one and two cigarettes. The levels of norharman and harman increased in plasma from smokers and nonsmokers. Ex vivo saturation kinetic experiments revealed that the baseline affinity constant of monoamineoxidase in platelets from smokers was higher than that of nonsmokers in contrast to the maximum turnover rate, which did not differ. Acute smoking affected the monoamineoxidase in nonsmokers only. It is discussed that inhibition of both isoforms of monoamineoxidase is necessary for the neuroprotection and that both norharman and harman play an important role.