The Effects of Methamphetamine on Oxidative Stress Markers in the Brain

In the last decade, prescription stimulants have gained popularity in young adults despite the potential adverse consequences. Amphetamine-like compounds, even at moderate doses, promote the production of reactive oxygen species via dopamine-dependent pathways. We hypothesized that late neurobehavioral deficits were caused by heightened oxidative stress as a response to early chronic exposure to methamphetamine. Four-month-old male and female mice were injected with either saline or methamphetamine twice a day for 4 weeks. After behavioral testing at 9-10 months of age, the mice were euthanized and brain regions were dissected (cortex, cerebellum, hippocampus, striatum, midbrain). These regions were used to measure markers of oxidative stress and dopaminergic function. Preliminary outcomes revealed that dopaminergic function was not majorly affected by methamphetamine treatment, whereas lipid peroxidation levels were increased in the cerebellum of males and in the cortex and midbrain of females. These preliminary results suggest that early chronic methamphetamine administration induced changes in oxidative stress, and more so in the females than the males. These data indicate possible long-term consequences on functional and biochemical changes that will be examined in future studies.