The Contribution of cocoa additive to cigarette smoking addiction

RIVM report 650270002 Page 153 of 207
Phenylethylamine
oxidase upon the cerebral circulatory and metabolic actions of phenylethylamine
were examined. The reductions in cerebral blood flow (28 percent) and cerebral
oxygen consumption (31 percent) that accompany the intracarotid administration of
phenylethylamine (0.25 mg/kg/min) were unaffected by the prior administration of
either phenoxybenzamine (1.5 mg/kg, iv) or pimozide (0.5 mg/kg, iv). The
administration of phenoxybenzamine and pimozide per se did not significantly
disturb cerebral blood flow or oxygen consumption. The ability of migraine patients
to oxidatively deaminate phenylethylamine is reduced at the time of their attacks. In
the present experiments, the administration of the monoamine oxidase type B
inhibitor, deprenyl (1 mg/kg, iv), did not effect significant changes in cerebral blood
flow or cerebral oxygen consumption. However, following deprenyl, the
administration of phenylethylamine (5 µg/kg/min), a concentration which was
without effect in normal animals, significantly reduced cerebral blood flow (19).
Monoamine oxidase (MAO) is responsible for the pulmonary metabolism of
phenylethylamine. The effects of treatment of rats with the tricyclic antidepressant
desmethylimipramine (DMI) on the disposition phenylethylamine in isolated perfused
rat lungs was investigated. During a 10-min perfusion at a concentration of 10 -6 M
phenylethylamine were rapidly taken up and extensively metabolized by lungs from
control animals. Phenylethylamine clearance in perfused lung was decreased in a
dose-related manner by DMI treatment with a corresponding decrease in its
metabolism. In efflux experiments, unmetabolized phenylethylamine was only found
in the perfusate from lungs of DMI-treated rats. It was concluded that
phenylethylamine clearance after DMI results almost entirely from inhibition of
pulmonary MAO. The data also suggest that there may be two discrete pools of MAO
in lung, one of which is relatively unaffected by DMI (21).
Critical assessment
Chemical
Phenylethylamine can react with aldehydes and cyanides. Adducts formed with other
cigarette components have MAO inhibitory properties.
In vivo
Phenylethylamine shows an interaction with monoamine oxidase inhibitors (MAOI).
The MAO-I increases the phenylethylamine level in the body. It is plausible that
phenylethylamine availability from cigarette smoking will be increased when MAO is
inhibited.
Conclusion
Chemical
Phenylethylamine can react with aldehydes and cyanides in cigarettes and the formed
adducts can inhibit MAO.
In vivo
MAO is responsible for the metabolism of phenylethylamine. Therefore, MAO-I
increases phenylethylamine level in the body.
DEPENDENCY
Phenylethylamine is an endogenous brain amine, which has been characterised as an
endogenous amphetamine. The rewarding properties of the structurally similar drug
amphetamine in humans and other species indicate a possible role for endogenous