Sixtus, 14.12.2005 15:25:
Pistäpääs sinä puolestas jotain lähdelinkkiä, jossa todetaan MDMA:n olevan ihmiselle heroiinia vaarallisempaa. Lukisin mielelläni. Mun tietojeni perusteella MDMA:n pysyviä haittavaikutuksia aivoille ei edelleenkään ole pystytty tieteellisesti täysin todistamaan, mutta mikäli tämä tieto on jo vanhentunutta, päivittäisin mielelläni tietoni tämän asian suhteen.
Huomaa etten tarkoittanut että MDMA on
vaarallisempaa kuin heroiini vaan
myrkyllisempää. Ts. heroiinia tarvi vähemmän kuollakseen kuin MDMA:ta mutta MDMA aiheuttaa enemmän vaurioita. Opiaatit ovat ei-toksisia. MDMA:sta löytyy rutkasti tietoa, googlella löytää =) Ongelmana on se että tutkimukset antavat risririitoista tietoa.
Suurin osa nykytutkimuksista kyllä viittaa siihen että MDMA on neurotoksinen, myös pitkällä aikavälillä. Nämä tutkimukset ovat ainakin vakuuttaneet minut enemmän kuin ne jotka väittää painvastaista.
The existing data indicate that MDMA produces long-term deficits in markers of 5-HT axon terminals in the rodent brain. Increased cleavage of the cytoskeletal protein tau, impairment of axonal transport, and functional consequences associated with a 5-HT depleting regimen of MDMA support the view that MDMA induces structural brain damage, that is, axonal degeneration. A confluence of oxidative stress and bioenergetic stress induced by MDMA is hypothesized to underlie the process of MDMA neurotoxicity (Fig. 3). The actions of MDMA on the 5-HT transporter to promote free radical formation and/or intracellular calcium may synergize with MDMA-induced disturbances in cellular energetics and hyperthermia to effect selective toxicity to 5-HT axon terminals.
Lähde; Neuropharmacology and neurotoxicity of
3,4-methylenedioxymethamphetamine
by
Gudelsky GA, Yamamoto BK.
College of Pharmacy,
University of Cincinnati,
Cincinnati, OH, USA.
Methods Mol Med 2003;79:55-73
"Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) are amphetamine analogs with high abuse potential. These drugs also cause damage to dopamine and serotonin nerve terminals in vivo. The mechanisms by which these drugs cause neurotoxicity are not known, but a great deal of attention has been focused on reactive oxygen species (ROS) and reactive nitrogen species (RNS) as mediators of this toxicity. ROS and RNS have very short biological half-lives in vivo, and it is virtually impossible to measure them in brain directly. However, ROS and RNS are also characterized by their extreme reactivity with proteins and nucleotides. Tryptophan hydroxylase (TPH) and tyrosine hydroxylase (TH), the initial and rate limiting enzymes in the synthesis of serotonin and dopamine, respectively, are identified targets for the actions of METH and MDMA. Using recombinant forms of these proteins, we have found that nitric oxide, catechol-quinones, and peroxynitrite, all of which are potentially produced by the neurotoxic amphetamines, covalently modify both TPH and TH. The ROS and RNS cause reductions in catalytic function of these enzymes in a manner that is consistent with the effects of METH and MDMNA in vivo. Protein-bound ROS or RNS may serve as molecular footprints of neurotoxic amphetamine action."
Lähde:
Molecular footprints of neurotoxic amphetamine action
by
Kuhn DM, Geddes TJ
Department of Psychiatry and Behavioral Neurosciences,
Wayne State University School of Medicine, Detroit,
Michigan 48201, USA.
[email protected]
Ann N Y Acad Sci 2000; 914:92-103
http://www.neurotransmitter.net/mdmatoxicity.html (hyvä linkki jos jaksaa lukea!)
http://mdma.net/toxicity/
http://mdma.net/toxicity/neurotox.html
luulis et serotoniinsyndrooma ja ylilämpeneminen uhkaa helpommallakin...
