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Ibogaine – Pinoline
Pinoline is a methoxylated tryptoline (5-methoxytryptoline) long claimed to be produced in the pineal gland during the metabolism of melatonin, however its pineal occurrence remains ;Its IUPAC name is 6-methoxy-1,2,3,4-tetrahydro-β-carboline, usually abbreviated as 6-MeO-THBC, and its more common name is a combination of "pineal beta-carboline". The biological activity of this molecule is of interest as a potential free radical scavenger, also known as an antioxidant, and as a monoamine oxidase A inhibitor. Bausch & Lomb filed a patent for a drug delivery device utilizing this molecule, designed to treat various ophthalmic disorders in 2006. Pharmacology One of pinoline's most outstanding pharmacological properties is its ability to promote neurogenesis in vitro; even at trace concentrations. Aluminium toxicity causes an increase in lipid peroxidation, with most damage occurring in the brain. A recent review of studies shows pinoline and melatonin to be effective at reducing the lipid peroxidation. Studies included both human and animal subjects. The studies’ results support that pinoline has antioxidant properties. Lipopolysaccharide is produced by Gram-negative bacteria and stimulates the production of free radicals which in turn cause lipid peroxidation. A recent study compared the effectiveness of melatonin and other similar compounds on the lipopolysaccharide induced lipid peroxidation. The results showed support for pinoline’s ability to reduce damage from lipid peroxidation. Pinoline was also shown to be more effective than vitamin E at reducing lipopolysaccharide activity in the retina. Another recent study compared the antioxidant properties of compounds from the tryptophan metabolic pathway in the pineal gland against oxidative damage to the lipids and proteins of synaptosomes. Synaptosomes isolated from rat brains were used in an experiment assessing damage by measuring malondialdehyde, 4-hydroxyalkenal, and carbonyl content in…
Ibogaine Adverse effects
Immediate One of the first noticeable effects of large-dose ibogaine ingestion is ataxia, a difficulty in coordinating muscle motion which makes standing and walking difficult without ;Xerostomia (dry mouth), nausea, and vomiting may follow. These symptoms may be long in duration, ranging from 4 to 24 hours in some cases. Ibogaine is sometimes administered per rectum to avoid nausea and vomiting. Cardiovascular Ibogaine causes long QT syndrome at therapeutic doses, apparently by blocking hERG potassium channels in the heart. Neurotoxicity Work in the laboratory of Mark Molliver at Johns Hopkins indicated degeneration of cerebellar Purkinje cells observed in rats given substantially larger dosages of ibogaine than those used to study drug self-administration and ;However, subsequent research found no evidence of neurotoxicity in the primate or mouse at dosages that produced cerebellar degeneration in the rat, and it has been suggested that cerebellar degeneration might be a phenomenon limited to a single ;The FDA was aware of Molliver's work at the time it approved a Phase 1 study in which humans received ibogaine in ;Neuropathological examination revealed no evidence of degenerative changes in a woman who had received four separate doses of ibogaine ranging between 10 and 30 mg⁄ kg over a 15-month interval prior to her death due to a mesenteric artery thrombosis with small bowel infarction 25 days after her last ingestion of ;A published series of fatalities temporally associated with the ingestion of ibogaine found no evidence suggesting a characteristic syndrome of neurotoxicity.