N&PD Moderators: Skorpio | thegreenhand
the bromo-dfly wikipedia states:
"Also, a Swedish man had to have the front part of his feet and several fingers on one hand amputated after taking a massive overdose. Apparently the compound acted as a long-acting efficacious vasoconstrictor, leading to necrosis and gangrene which was delayed by several weeks after the overdose occurred. Several other cases have also been reported of severe peripheral vasoconstriction following overdose with Bromo-DragonFLY, and a similar case is also known from DOB"
is this true?
and why?
Explain how Nitrous Oxide is a NMDA antagonist.
Does N2O affect any other receptors/neurotransmitters in the brain?
How is N2O metabolized?
Is there a dangerous number of 8g chargers not to go over in a single dose? I've done 3 at the most, but was thinking I may want to try 4. Essentially, what is the LD50?
Can you be allergic to N2O?
Yes you can be allergic to just about anything so I doubt N2O is any exception.
In my personal experience, yes, it does.
Temperature and 3,4-methylenedioxymethamphetamine alter human serotonin transporter-mediated dopamine uptake
Shannon N. Saldaña and Eric L. Barker
Although studies have suggested that dopamine can be transported by serotonin transporters (SERTs), such activity has not been characterized at the cloned SERTs. Dopamine and serotonin uptake by human SERT expressed in HEK-293 cells was compared at 37 and 40 °C. Elevated temperature was found to alter serotonin transport, but had no significant effect on dopamine transport. These effects led to a 10-fold increase in the serotonin:dopamine transport ratio reflecting an increased preference of SERTs for dopamine as opposed to serotonin at the higher temperature. The effects of 3,4-methylenedioxymethamphetamine (MDMA) on SERT-mediated dopamine transport were also evaluated by pre-incubating SERT-expressing cells with MDMA. The presence of intracellular MDMA caused a decrease in [3H]dopamine uptake but had no effect on [3H]serotonin transport suggesting that intracellular MDMA may be capable of inhibiting transporter function.
Doesn't it also have a lot to do with the specific metabolites of the drug?eg methamphetamine, which is much more toxic than MDMA
Doesn't it also have a lot to do with the specific metabolites of the drug?
I don't think so. The main metabolites are p-OH-METH, p-AMP and p-OH-AMP. The hydroxylations I believe are mediated by hepatic P450 enzymes. The effect on catecholamines and serotonin (high amounts of radicals generated by MAO degredation under elevated temperatures destroying mitochondrial DNA and forming toxic metabolites of the endogenous neurotransmitters) is probably more responsible for the neurotoxic effect. I'd be willing to bet that any potent releaser of all three monoamines may cause neurotoxicity.
This indanylamphetamine, (also called IAP, 1-(5-Indanyl)-2-aminopropane or 5-(2-aminopropyl)indane) is an analog of MDA, but with both oxygens in the methylenedioxy bridge replaced by methylene (CH2) units. It has been shown to not be a serotonergic neurotoxin, and is active at 0.2 mg/kg in Nichols' lab rat tests, compared to 0.8 mg/kg for MBDB. However, the lab rat results show that the effects should be somewhere inbetween MDA and MBDB, as it doesn't fully substitute for the purely serotonergic compound MMA (3-Methoxy-4-Methyl- Amphetamine), but does share some of the dopaminergic effects of MDA. Further animal tests showed that IAP does not substitute for amphetamine, so the compound is not a particular stimulant either. IAP is also one of the most active serotonin-releasing agents known so far, together with the 4-iodoamphetamine and 4-methylthioamphetamine (4-MTA). However, 4-iodoamphetamine is a serotonergic neurotoxin, and 4-methylthioamphetamine has also shown signs of toxicity, as it also exhibit MAOI properties. This together with is serotonin-releasing properties, makes it prone to give a serotonin syndrome in people taking it, and several 4-MTA related deaths has been reported. The same cannot be ruled out for IAP, so caution is advised in any human testing of this compound. The animal test results suggest that the active dose is somewhere between 20-40mg. In October 1998, there were news reports that the compound had been seized together with other ecstasy-like compounds in South Australia (possibly Adelaide), confirming that it has been manufactured in clandestine laboratories there.
Naphthylisopropylamine (PAL-287), or naphthylaminopropane (NAP), is a psychoactive drug and research chemical currently under development for the treatment of alcohol and stimulant drug addiction. It functions as a non-neurotoxic and well-proportioned serotonin, norepinephrine, and dopamine releasing agent.[1]