Bufotenine is also known as bufotenin, dimethyl serotonin, 5-OH-dimethyltryptamine (5-OH-DMT), N,N-dimethyl-5-hydroxytryptamine, and mappine. The name bufotenine was suggested in 1893 by the French scientists Césaire Auguste Phisalix (1852-1906) and Gabriel Bertrand (1867-1962), and officially introduced in 1920 by the Austrian chemist Hans Handovsky (1888-1959) as the name of a chemical substance isolated by him from toadskin. The name derives from the Bufo genus of toads, various species of which secrete a complex mixture of psychoactive substances that includes bufotenine. Bufotenine also occurs in the eggs of toads such as Bufo alvarius and Bufo marinus,as well as in the Amazonian-Antillean narcotic snuff Anadenanthera peregrina, and in some mushrooms, higher plants, and animals.Because of their psychoactive excrements, animals such as B. alvarius and B. marinus are referred to as * psychoactive fauna. Although bufotenine was not isolated until 1920, toad secretion has been used as an * entheogen by shamans and mystics since ancient times. Its toxicity was recorded as early as the first century AD by the Roman poet Decimus Junius Juvenal (AD 60-128). Today bufotenine is classified as a hallucinogenic tryptamine from the group ofindole alkaloids. Its chemical structure, which is related to that ofthe * hallucinogens psilocin and dimethyltryptamine (DMT), as well as to that of the neurotrans-mitter serotonin, was discovered in 1934 by the group of the German chemist and Nobel prize laureate Heinrich Otto Wieland (1877-1957).
In 1935-1936 bufotenine was synthesized for the first time by the Japanese chemists Toshio Hoshino and Kenya Shimodaira. Because orally ingested bufotenine is rapidly inactivated by the body's monoamine oxidase (MAO) system, it is usually applied intranasally, intravenously, by inhalation, or in the form of an enema. For recreational use, bufotoxins are also ingested by means of toad licking. For bufotenine to be biologically effective, the latter technique requires the simultaneous use of a MAO-inhibiting substance such as tranylcypromine to prevent a premature inactivation of bufotenine. The hallucinations mediated by bufotenine intoxication are described as predominantly visual in nature.
*Simple and * geometric visual hallucinations, in particular, have been reported, as well as * trailing phenomena and an increased intensity of colours. Intense visual and * auditory hallucinations have been reported as well, however, commencing seconds after inhaling the smoke of dried toad venom, and lingering on for about 5 min. Traditionally comparisons have been made with the effects of other hallucinogens such as LSD and mescaline, although the effects of bufotenine are reported as being milder, and of a shorter duration. Due to the presence of the other toxins in Bufo toad venom and eggs, the oral ingestion of these substances may induce various unexpected side effects. Occasionally it may even result in epileptic seizures, coma, and eventually death.
References
Handovsky, H. (1920). Ein Alkaloid in Gifte von Bufo vulgaris. Archiv für Experimentelle Pathologie und Pharmakologie, 86, 138-158.
Rudgley, R. (1998). The encyclopaedia ofpsy-choactive substances. London: Little, Brown and Company.