d-MDMA during vitamin E deficiency: effects on dopaminergic neurotoxicity and hepatotoxicity

Brain Research
Elizabeth Anne JohnsonDiane B Miller

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 sever...Continue Reading

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Jan 11, 2005·Neurotoxicity Research·H G Baumgarten, L Lachenmayer
Mar 7, 2012·Archives of Toxicology·Márcia CarvalhoMaria de Lourdes Bastos
Apr 15, 2004·Psychopharmacology·M Isabel ColadoA Richard Green
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