The Contribution of cocoa additive to cigarette smoking addiction

RIVM report 650270002 Page 119 of 207
Tryptamine
potent inhibitor of protein biosynthesis, via the competitive inhibition of
tryptophanyl-tRNA synthetase (TrpRS). The results indicate that long-term
tryptamine treatment of HeLa cells led to a significant increase in the half-life of
TrpRS. It was shown that tryptamine is an effective inhibitor of HeLa cell growth. In
contrast to the well-characterized antineoplastic compounds, resistance to tryptamine
at very low levels was difficult to achieve, i.e. the 2-fold resistant subline was
selected after 19 months of treatment of HeLa cells with gradually increasing
concentrations of tryptamine. It was suggested that tryptamine could be a potential
anti-cancer drug (55).
Critical assessment
Not relevant.
Conclusion
Not relevant.
SUMMARY AND FINAL CONCLUSION
The natural amount of tryptamine in tobacco leaves is at least 5000 times higher than
the tryptamine amount from added cocoa to tobacco. Therefore, it is debatable
whether tryptamine should be considered as an additive to tobacco. The daily intake
of tryptamine from cigarettes (from tobacco leaves and from added cocoa) is is higher
than the intake from other sources, like chocolate or tomato. Assuming similar
bioavailability, the plasma concentration reached after ingestion of tryptamine from
chocolate sources or other food sources is expected to be lower, than after exposure
from cigarettes. No conclusion can be drawn about the amount of tryptamine in
cigarettes compared with the amount present in mammalian body.
Tryptamine is a neurotransmitter or a modulator of neurotransmission. Tryptamine
produces pharmacological effects in man that are similar to LSD and other tryptamine
derivatives. Such effects are tachypnea, tachycardia, behavioral changes and
hallucinations. Experiments with rats showed that tryptamine evoke effects, which
are related to serotonin receptors. It has a biphasic effect on the arterial tone,
induction of acquisition deficit, hypothermia and anorectic effect and affected the
glucose plasma level. The tryptamine dose used to show these effects were in the
range of 1 µg/dose (i.c.v.) and 5 mg/kg body weight (ipr.). However, no data are
available on tryptamine pharmacological effects by respiratory studies. It is not clear
whether the estimated potential tryptamine dose in cigarette (1000 µg/day) exerts any
respiratory effects, as only data are available via other routes.
Little is known about tryptamine pharmacokinetics in man from respiratory studies on
tryptamine. It seems that oral tryptamine is inactive and tryptamine level in the brain
is affected by tryptophan load. Tryptamine is synthesised by amino acid
decarboxylase (AAD) from tryptophan in several tissues. The major route of
catabolism for tryptamine is one of enzymatic inactivation. Tryptamine is excreted in
the urine after oral loading with L-tryptophan.
Tryptamine produces pharmacological effects in man which are similar to those
produced by LSD, mescaline, psilocin and other tryptamine derivatives. These
effects include tachycardia, tachypnea, mydriasis, hyperreflexia, behavioral changes
and in man, hallucinations. No toxicological data are available from tryptamine
inhalation studies. Intravenous data on tryptamine in rats, indicate that 15 mg/kg dose