The Contribution of cocoa additive to cigarette smoking addiction

RIVM report 650270002 Page 135 of 207
Tyramine
when smoke from cigarettes with higher tar and nicotine content was used. When the
amines were incubated with human saliva obtained after cigarette smoking,
cyanomethylamine products were readily detected (41).
In vivo
The potentially fatal consequences of ingesting tyramine whilst receiving therapy
with monoamine oxidase inhibitors have been well documented. In normal subjects,
tyramine is rapidly inactivated by monoamine oxidase, but when the enzyme is
inhibited, tyramine can cause hypertensive crises by its indirect sympathomimetic
actions (1). Some monoamine oxidase inhibitors are moclobemide (18) and
toloxatone (42), brofaromine, clorgyline, selegiline, phenelzine, tranylcypromine
(43). In healthy volunteers, both propanolol and indenolol reduced the pressor
response to tyramine, as shown by a significant increase in the dose of tyramine
(effective dose) required to increase systolic blood pressure by 15% (ED15). The ED15
(i.v., bolus injection) was 2.2 mg prior treatment and 5.5 mg and 5.2 mg respectively
for indelol and propanolol (44).
Critical assessment
Chemical
The free amino group is
a potential group to react with aldehydes and ketones and with monoaminooxydase
(MOA);
a base group, i.e. a potential group to react with acids.
The phenolic hydroxyl group is a potential protondonor.
In vivo
The bioavailability of tyramine is affected by monoamine oxidase inhibitors. Antihypertension
drugs reduced the pressor response to tyramine.
Conclusion
Chemical
Tyramine contains two reactive sites of different nature: the aliphatic aminogroup
(base) and the phenolic hydroxylgroup (slightly acidic).
In vivo
Tyramine shows an interaction with monoamine oxidase inhibitors and antihypertension
drugs.
DEPENDENCY
No data available.
Effects of smoking cessation
No data available.
Critical assessment
Not possible.
Conclusion