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Vol. 287, Issue 1, 107-114, October 1998
Program in Basic and Clinical Neuroscience, Department of
Psychiatry, Case Western Reserve University School of Medicine,
Cleveland, Ohio
The effects of methamphetamine (METH) on pro-oxidant processes and on
the production of reactive oxygen species were examined in
vivo in the rat brain. The presence of oxidative damage in striatum, as revealed by the oxidation of lipid, also was assessed via the measurement of the lipid peroxidation product
malonyldialdehyde. To elucidate further the mechanisms mediating
METH-induced oxidative stress, we studied the possible reversal of the
long-term METH-induced decrease in striatal dopamine content by
antioxidants through iron chelation and trapping of free radicals. The
uric acid concentration in the striata of rats killed 1 hr, but not 24 hr, after a four-injection regimen of METH was increased significantly
compared with saline-injected control rats. METH increased the in
vivo formation of the hydroxylated products of salicylate and
d-phenylalanine, as evidenced by the elevated extracellular
concentrations of 2,3 dihydroxybenzoic acid and p-tyrosine,
respectively. The local perfusion of the striatum with the iron
chelator deferroxamine attenuated the long-term depletions of striatal
dopamine content produced by METH. In other experiments,
malonyldialdehyde concentrations in incubated striatal homogenates were
elevated significantly in METH-treated rats. Finally, pretreatment with
the spin trapping agent phenylbutylnitrone before the METH injections
attenuated the subsequent long-term depletions in striatal dopamine
content. Overall, the results illustrate that METH increases
pro-oxidant processes and offer supportive evidence that METH produces
oxidative damage. These studies also demonstrate that iron may be
involved in mediating the long-term damage to dopamine neurons after
repeated administrations of METH.
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