Analysis of information sources in references of the Wikipedia article "Mescaline" in English language version.
The low affinity of mescaline for 5-HT2A receptors [3] and poor blood–brain barrier permeability [20] contribute to the comparatively high oral doses of 300–800 mg of mescaline hydrochloride (HCl) that are typically required to induce a full psychedelic experience in humans compared with psilocybin dihydrate (20–40 mg) and LSD base (100–200 µg) [5, 21]. [...] We found that acute subjective efects of mescaline were closely linked to the plasma mescaline concentrations but occurred with a delay as seen in the counterclockwise hysteresis. Accordingly, our modeling approach that used an efect compartment that was connected to the plasma mescaline concentration using a frst-order equilibrium rate constant (ke0) adequately described the observed acute efects. This finding is consistent with a delayed central distribution of mescaline.
{{cite book}}: |journal= ignored (help)Some authors (398) postulated that mescaline oxidase is identical with diamine oxidase, while others (399-401) believe that the oxidative deamination of mescaline can be effected by monoamine oxidase or diamine oxidase or both. However, mescaline was found to be a poor substrate for highly purified human plasma monoamine oxidase (402) and for dopamine-β-oxidase (403). According to Seiler (404), who treated mescaline with mouse brain homogenates, the oxidation is not caused by diamine oxidase but by a monoamine oxidase leading to 3,4,5-trimethoxyphenylacetic acid (LXXIII). [...] rabbit liver preparations caused O-demethylation to VII and LX along with oxidation to LXXIII (407). The formation of this acid (LXXIII) was inhibited by iproniazid, semicarbazide, nicotinamide, and triphosphopyridine nucleotide. [...] Harmine was found to augment the effect of mescaline (260). [...] (260) H. Hoshikawa, Nippon Yakurigaku Zasshi, 58, 241, 261 (1962); through Chem. Abstr., 60, 7338(1964).
Mescaline (11a in Fig. 4) is known to be metabolized very slowly in humans, with more than 87 % of the ingested dose being excreted [...] with the urine within 24 h [36].
Some authors (398) postulated that mescaline oxidase is identical with diamine oxidase, while others (399-401) believe that the oxidative deamination of mescaline can be effected by monoamine oxidase or diamine oxidase or both. However, mescaline was found to be a poor substrate for highly purified human plasma monoamine oxidase (402) and for dopamine-β-oxidase (403). According to Seiler (404), who treated mescaline with mouse brain homogenates, the oxidation is not caused by diamine oxidase but by a monoamine oxidase leading to 3,4,5-trimethoxyphenylacetic acid (LXXIII). [...] rabbit liver preparations caused O-demethylation to VII and LX along with oxidation to LXXIII (407). The formation of this acid (LXXIII) was inhibited by iproniazid, semicarbazide, nicotinamide, and triphosphopyridine nucleotide. [...] Harmine was found to augment the effect of mescaline (260). [...] (260) H. Hoshikawa, Nippon Yakurigaku Zasshi, 58, 241, 261 (1962); through Chem. Abstr., 60, 7338(1964).
[...] there is circumstantial evidence for traditional use of ayahuasca containing mescaline and/or other β-phenethylamines in Amazonian Peru. [...] preliminary human bioassays suggest that the β-carboline harmaline might in fact potentiate mescaline - low doses of 60 and 100 mg mescaline hydrochloride, corresponding to 51 and 86 mg base or 0.78 and 1.32 mg/kg respectively, were decidedly psychoactive. The combination of mescaline or mescaline-containing cacti with β-carbolines has been dubbed peyohuasca.(5,18)
The low affinity of mescaline for 5-HT2A receptors [3] and poor blood–brain barrier permeability [20] contribute to the comparatively high oral doses of 300–800 mg of mescaline hydrochloride (HCl) that are typically required to induce a full psychedelic experience in humans compared with psilocybin dihydrate (20–40 mg) and LSD base (100–200 µg) [5, 21]. [...] We found that acute subjective efects of mescaline were closely linked to the plasma mescaline concentrations but occurred with a delay as seen in the counterclockwise hysteresis. Accordingly, our modeling approach that used an efect compartment that was connected to the plasma mescaline concentration using a frst-order equilibrium rate constant (ke0) adequately described the observed acute efects. This finding is consistent with a delayed central distribution of mescaline.
{{cite book}}: |journal= ignored (help)Some authors (398) postulated that mescaline oxidase is identical with diamine oxidase, while others (399-401) believe that the oxidative deamination of mescaline can be effected by monoamine oxidase or diamine oxidase or both. However, mescaline was found to be a poor substrate for highly purified human plasma monoamine oxidase (402) and for dopamine-β-oxidase (403). According to Seiler (404), who treated mescaline with mouse brain homogenates, the oxidation is not caused by diamine oxidase but by a monoamine oxidase leading to 3,4,5-trimethoxyphenylacetic acid (LXXIII). [...] rabbit liver preparations caused O-demethylation to VII and LX along with oxidation to LXXIII (407). The formation of this acid (LXXIII) was inhibited by iproniazid, semicarbazide, nicotinamide, and triphosphopyridine nucleotide. [...] Harmine was found to augment the effect of mescaline (260). [...] (260) H. Hoshikawa, Nippon Yakurigaku Zasshi, 58, 241, 261 (1962); through Chem. Abstr., 60, 7338(1964).
Mescaline (11a in Fig. 4) is known to be metabolized very slowly in humans, with more than 87 % of the ingested dose being excreted [...] with the urine within 24 h [36].
The low affinity of mescaline for 5-HT2A receptors [3] and poor blood–brain barrier permeability [20] contribute to the comparatively high oral doses of 300–800 mg of mescaline hydrochloride (HCl) that are typically required to induce a full psychedelic experience in humans compared with psilocybin dihydrate (20–40 mg) and LSD base (100–200 µg) [5, 21]. [...] We found that acute subjective efects of mescaline were closely linked to the plasma mescaline concentrations but occurred with a delay as seen in the counterclockwise hysteresis. Accordingly, our modeling approach that used an efect compartment that was connected to the plasma mescaline concentration using a frst-order equilibrium rate constant (ke0) adequately described the observed acute efects. This finding is consistent with a delayed central distribution of mescaline.
Santana at Woodstock, 1969 - Mescaline