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CopyrightYear: 2002
Johnson EA, Shvedova AA, Kisin E, O'Callaghan JP, Kommineni C, Miller DB. 
“d-MDMA during vitamin E deficiency: effects on dopaminergic neurotoxicity and hepatotoxicity”. 
Brain Res. 2002;933(2):150-163.
Abstract
The mechanism of 3,4-methylenedioxymethamphetamine d-MDMA-induced neurotoxicity may involve formation of toxic radical species. Endogenous defenses against toxic radical species include tissue stores of vitamin E, and thiols. We examined whether vitamin E deficiency could alter d-MDMA-induced neurotoxicity by administration of the drug to animals with diet induced vitamin E deficiency. Brain vitamin E levels in deficient mice were reduced 75 compared to sufficient animals. Animals received d-MDMA 5 or 10 mg/kg or saline delivered every 2 hx4, s.c.. Diet slightly altered d-MDMA-induced temperature modulation. In brain, MDMA treatment reduced vitamin E, total antioxidant reserve and protein thiols 72 h after the first dose. In liver, MDMA treatment reduced glutathione and total antioxidant reserve at the same time point. The vitamin E-deficient group, treated with the low dose of d-MDMA, exhibited neurotoxic responses, including reduced striatal dopamine 47 and elevated GFAP protein 3-fold: while the sufficient diet group was not altered. The higher d-MDMA dose caused neurotoxic responses in both diet groups. Liver toxicity was determined by histopathologic examination. d-MDMA caused hepatic necrosis that was more severe in vitamin E deficient than sufficient mice. These data indicate that 1 d-MDMA administration reduces antioxidant measures at a time coincident with d-MDMA-induced neuronal damage and 2 vitamin E deficiency increases susceptibility to d-MDMA-induced neurotoxicity and hepatic necrosis.
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