PMID- 16808729
OWN - NLM
STAT- MEDLINE
DCOM- 20070329
LR  - 20191110
IS  - 0892-0915 (Print)
IS  - 0892-0915 (Linking)
VI  - 17
IP  - 2
DP  - 2005
TI  - Amphetamine neurotoxicity: cause and consequence of oxidative stress.
PG  - 87-117
AB  - Oxidative stress has been demonstrated to occur in response to high doses of 
      substituted amphetamines such as methamphetamine (METH) and 
      3,4-methlyene-dioxymethamphetamine (MDMA). This term represents a set of complex 
      and multi-faceted precursor events that occur in both a parallel and serial 
      manner, eventually converging to produce oxidative damage. This critical review 
      goes beyond the compilation of previously well-documented evidence demonstrating 
      that oxidative stress mediates METH and MDMA toxicity to dopamine and/or 
      serotonin nerve terminals. The diverse causes, effects, and impact of 
      pro-oxidative processes produced by these drugs are highlighted, integrated, and 
      assembled into a proposed temporal sequence in an effort to explain the long-term 
      neurochemical changes produced by amphetamines. Multiple factors are considered, 
      including dopamine, glutamate, impaired mitochondrial bioenergetics, and 
      inflammatory processes, all of which converge and are necessary but alone may be 
      insufficient to cause damage to dopamine and/or 5-HT terminals. In addition, the 
      processes linking inflammation and oxidative stress are considered and described 
      as a feedforward process. The self-perpetuating cycle of inflammation and 
      oxidative stress that is initiated by dopamine, glutamate, and mitochondrial 
      dysfunction may extend well beyond the acute pharmacodynamic effects of the drugs 
      and could represent an underlying and potentially progressive degenerative 
      process.
FAU - Yamamoto, Bryan K
AU  - Yamamoto BK
AD  - Department of Pharmacology, Laboratory of Neurochemistry, Boston University 
      School of Medicine, Boston, MA 02118, USA. bkyam@bu.edu
FAU - Bankson, Michael G
AU  - Bankson MG
LA  - eng
GR  - DA07606/DA/NIDA NIH HHS/United States
GR  - DA16501/DA/NIDA NIH HHS/United States
GR  - DA16866/DA/NIDA NIH HHS/United States
GR  - DA7427/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - United States
TA  - Crit Rev Neurobiol
JT  - Critical reviews in neurobiology
JID - 8710803
RN  - 0 (Amphetamines)
RN  - 333DO1RDJY (Serotonin)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Amphetamines/*toxicity
MH  - Animals
MH  - Brain/*drug effects/pathology
MH  - Dopamine/metabolism
MH  - Humans
MH  - Inflammation/pathology/physiopathology
MH  - Mitochondria/drug effects/pathology
MH  - Nerve Endings/*drug effects/pathology
MH  - Neurotoxicity Syndromes/*physiopathology
MH  - Oxidative Stress/*drug effects
MH  - Serotonin/metabolism
RF  - 268
EDAT- 2006/07/01 09:00
MHDA- 2007/03/30 09:00
CRDT- 2006/07/01 09:00
PHST- 2006/07/01 09:00 [pubmed]
PHST- 2007/03/30 09:00 [medline]
PHST- 2006/07/01 09:00 [entrez]
AID - 04c698ea6529efba,51741a1b2a4b5a60 [pii]
AID - 10.1615/critrevneurobiol.v17.i2.30 [doi]
PST - ppublish
SO  - Crit Rev Neurobiol. 2005;17(2):87-117. doi: 10.1615/critrevneurobiol.v17.i2.30.