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. (C) 2000 Elsevier Science B.V.
|Number of pages||5|
|State||Published - Sep 29 2000|
Bibliographical noteFunding Information:
This work was supported by USPHS Grants NS 01941 to WFM, CA 59835 to DKS, DA 10115 to WAC and AG 10836 to DAB. Electron micrographs were obtained using the University of Kentucky’s Image Facility with the assistance of Ms. Mary Gail Engle.
- Manganese superoxide dismutase
- Oxidative stress
- Transgenic mouse
ASJC Scopus subject areas
- Neuroscience (all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology