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Voluntary exercise protects against methamphetamine‐induced oxidative stress in brain microvasculature and disruption of the blood‐brain barrier
Author(s) -
Toborek Michal,
Seelbach Melissa J.,
Choi Yean Jung,
András Ibolya E.,
Chen Lei,
Hennig Bernhard,
Esser Karyn A.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1020.7
Subject(s) - meth , methamphetamine , occludin , oxidative stress , blood–brain barrier , cerebral blood flow , medicine , pharmacology , brain damage , toxicity , nadph oxidase , central nervous system , chemistry , tight junction , biochemistry , acrylate , polymer , monomer , organic chemistry
Moderate to vigorous exercise is a powerful means to influence health status and lower the risk of the development of chronic diseases. We hypothesize that increased antioxidant potential by endurance exercise plays a critical role in the protection against the development of cerebral toxicity associated with drug abuse. To address this hypothesis, mice were subjected to voluntary wheel running for 5 weeks. The control mice did not have access to running wheels. At the end of exercise training, mice were injected with methamphetamine (Meth, 10 mg/kg) for 24 h. Exercise markedly changed Meth‐induced alterations of cerebral blood flow and protected against Meth‐induced disruption of the blood‐brain barrier as assessed by in‐situ brain perfusion. Consistent with these results, exercise protected against Meth‐mediated disruption and localizations of tight junction protein expression (ZO‐1, occludin, and claudin‐5). Importantly, exercise markedly attenuated Meth‐induced oxidative stress in brain microvessels. It appears that protection against upregulation of NADPH oxidase may be responsible, at least in part, for these protective effects. The obtained results indicate that exercise is an important modifiable behavioral factor that can protect against Meth‐induced CNS toxicity. Supported by MH63022, MH072567, NS39254, and from the University of Kentucky Center for Muscle Biology.