PMID- 15639791
OWN - NLM
STAT- MEDLINE
DCOM- 20050408
LR  - 20230320
IS  - 1029-8428 (Print)
IS  - 1029-8428 (Linking)
VI  - 6
IP  - 7-8
DP  - 2004
TI  - Serotonin neurotoxins--past and present.
PG  - 589-614
AB  - Autoxidation pathways and redox reactions of dihydroxytryptamines (5,6- and 
      5,7-DHT) and of 6-hydroxydopamine (6-OH-DA) are illustrated, and their potential 
      role in aminergic neurotoxicity is discussed. It is proposed that certain aspects 
      of the cytotoxicity of 6-OH-DA and of the DHTs, namely redox cycling of their 
      quinone- and quinoneimine-intermediates as a source of free radicals, may also 
      apply to quinoidal reactive intermediates and to glutathionyl- or cysteinyl 
      conjugates ("thioether adducts") of o-dihydroxylated (catechol-like) metabolites 
      of certain substituted amphetamines (of methylenedioxymethamphetamine (MDMA) and 
      of methylenedioxyamphetamine (MDA)). Despite similarities in their primary 
      interaction with the plasmalemmal (serotonergic transporter/dopamine transporter, 
      SERT/DAT) and vesicular monoamine transporters (VMAT2), MDMA and fenfluramine 
      (N-ethyl-meta-trifluoromethamphetamine, Fen) differ substantially in many aspects 
      of their metabolism, pharmacokinetics, pharmacology, and neurotoxicology profile; 
      the consequences of these differences for neuronal response patterns and 
      long-term survival prospects are not yet fully understood. However, sustained 
      hyperthermia appears to be a critical factor in these differences. Methodological 
      requirements for adequate detection and description of pre- and postsynaptic 
      forms of drug-induced neurotoxicity are exemplified using recently published 
      accounts. The inclusion of microglial markers into research strategies has 
      widened contemporary pathogenetic concepts on methamphetamine (MA)-induced 
      neurotoxicity as an example of inflammatory neurodegeneration, thus complementing 
      the traditional ROS and RNS-dependent stress models. Amphetamine-type 
      neurotoxicity studies may assist in elaborating of preventive strategies for 
      human neurodegenerative disorders.
FAU - Baumgarten, H G
AU  - Baumgarten HG
AD  - Institut fur Anatomie, Charite Universitatsmedizin Berlin, Campus Benjamin 
      Franklin, Konigin-Luise-Str. 15, 14195 Berlin, Germany. 
      hans-georg.baumgarten@charite.de
FAU - Lachenmayer, L
AU  - Lachenmayer L
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
RN  - 0 (Neurotoxins)
RN  - 333DO1RDJY (Serotonin)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Neurons/drug effects/metabolism
MH  - Neurotoxins/*toxicity
MH  - Serotonin/analogs & derivatives/*metabolism/*toxicity
RF  - 210
EDAT- 2005/01/11 09:00
MHDA- 2005/04/09 09:00
CRDT- 2005/01/11 09:00
PHST- 2005/01/11 09:00 [pubmed]
PHST- 2005/04/09 09:00 [medline]
PHST- 2005/01/11 09:00 [entrez]
AID - 10.1007/BF03033455 [doi]
PST - ppublish
SO  - Neurotox Res. 2004;6(7-8):589-614. doi: 10.1007/BF03033455.