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AP-1 DNA-binding activation by methamphetamine involves oxidative stress.

P Sheng·X B Wang·B Ladenheim·C Epstein·J L Cadet
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Abstract

Methamphetamine (METH) caused dose-dependent increases in AP-1 DNA-binding activity in both nontransgenic (Non-Tg) and CuZn-SOD transgenic (SOD-Tg) mice. However, the increases in SOD-Tg mice were less prominent than those observed in Non-Tg animals. The time-course of METH-induced AP-1 changes was similar in both strains of mice. AP-1 binding activity showed an initial increase at 1 h, peaked at 3 h, and then gradually declined. AP-1 binding activity was back to normal by the 72-h time point. Regional analyses of METH effects revealed increases in the caudate putamen and cerebellum, with the striatum showing relatively higher METH-induced AP-1 DNA-binding activation. These regional effects were also attenuated in the SOD-Tg mice. These data indicate that METH-induced stimulation of AP-1 DNA-binding depends on cellular redox status. These results are consistent with in vitro studies that have reported that several transcription factors are regulated through redox mechanisms.

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AnimalsBrain ChemistryCentral Nervous System StimulantsDNAElectrophoresis, Polyacrylamide GelHumansKineticsMethamphetamineMiceMice, TransgenicOxidative StressSuperoxide DismutaseTranscription Factor AP-1Journal Article

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P Sheng, X B Wang, B Ladenheim, C Epstein, J L Cadet. 1996. AP-1 DNA-binding activation by methamphetamine involves oxidative stress.. https://doi.org/10.1002/(sici)1098-2396(199611)24%3A3%3C213%3A%3Aaid-syn2%3E3.0.co%3B2-h

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