Methamphetamine toxicity is attenuated in mice that overexpress human manganese superoxide dismutase.
We have investigated methamphetamine (MA) toxicity in transgenic mice that overexpress the human form of mitochondrial manganese superoxide dismutase (MnSOD). Our results reveal a significant reduction in the long-term depletion of striatal dopamine and protein oxidation following repeated administration of MA in transgenic vs. non-transgenic littermates. These findings support the notion that ROS contribute to MA-induced brain damage and suggest that mitochondria may play an important role in this form of neurodegeneration.
Maragos
W F
WF
Department of Neurology, Kentucky Clinic, Room L-445, University of Kentucky, Lexington, KY 40536-0284, USA. maragos@pop.uky.edu
Jakel
R
R
Chesnut
D
D
Pocernich
C B
CB
Butterfield
D A
DA
St Clair
D
D
Cass
W A
WA
D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D008694:Methamphetamine / Q000037:antagonists & inhibitors* / Q000506:poisoning*; D051379:Mice; D008822:Mice, Transgenic / Q000235:genetics; D008928:Mitochondria / Q000201:enzymology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D012016:Reference Values; D013482:Superoxide Dismutase / Q000235:genetics / Q000494:pharmacology*
D009419:Nerve Tissue Proteins; D008694:Methamphetamine; D013482:Superoxide Dismutase; D004298:Dopamine