The Contribution of cocoa additive to cigarette smoking addiction

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Page 168 of 207 RIVM report 650270002 Octopamine is high in the body. Octopamine is excreted in conjugated and unconjugated form. Conclusion There are no in-vivo pharmacokinetic data available on respiratory intake of octopamine in human. Based on in-vivo metabolism data, probably pulmonary MAO will reduce the bioavailability of octopamine through cigarette smoking. TOXICOLOGY Acute toxicity Human No data available. Animal rat oral LD50: 1240 mg/kg (1) rat ipr. LD50: 1350 mg/kg (1) rat scu LD50: 350 mg/kg (1) mouse oral LD50: 4200 mg/kg (1) mouse ipr. LD50: 600 mg/kg (1) mouse scu. LD50: 2070 mg/kg (1) mouse iv. LD50: 75 mg/kg (1) guinea pig iv.LDLo: 200 mg/kg (1) Octopamine administered to rats in doses of 50, 100 and 250 µg into the cerebral ventricles exerted a stimulating effect on the dopaminergic structures in the rat brain. In doses of 100 and 250 µg octopamine also had an anticataleptic effect (38). Local tolerance Human No data available. Animal No data available. Repeated dose toxicity Subacute No data available. Semichronic No data available. Chronic No data available. Carcinogenicity Human No data available. Animal No data available.
RIVM report 650270002 Page 169 of 207 Octopamine Reproduction toxicology Human No data available. Animal No data available. Mutagenicity Human No data available. Animal No data available. Other Critical assessment No human toxicological data are available on octopamine inhalation. Mainly animal LD50 data are available. Conclusion No data are available on octopamine toxicological effects in human. INTERACTIONS Chemical Octopamine undergoes self-condensation between 155 ºC and 190 ºC in which the two amine groups yield 2,5-diaryl-piperazine derivative, with loss of two molecules of water (39). In vivo The effect of octopamine (0.158 – 15.8 µM) on the twitch responses of the prostatic portion of the rat vas deferens to electrical stimulation (0.025 Hz) was affected by inhibitor (praglyline) of monoamine oxidase (MAO) activity and antagonists of α1and α2-adrenoceptors (corynanthine and yohimbine), respectively. Pretreatment with reserpine (5 mg/kg, 24 h; 2.5 mg/kg, 2 h before the experiment) largely prevented the effects of p-octopamine, but the amine still modified the twitch responses to field stimulation. Cocaine (10 µM) did not antagonize, but rather enhanced the inhibitory effects of p-octopamine in tissues with normal contents of noradrenaline (40). The MAO-inhibitors and α-adrenergic antagonist seems to affect octopamine turnover in the mammalian brain (41, 42). Octopamine (50 and 250 µg ivc) potentiated the tremorine (10 mg/kg ip) induced hypothermia in the rat. This effect was partially antagonized by atropine (10 mg/kg ip). Octopamine significantly prolonged the duration of pilocarpine (100 mg/kg iv) induced catalepsy in rats (43).
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