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Protective effects of N-acetylcysteine on 3, 4-methylenedioxymethamphetamine-induced neurotoxicity in male Sprague-Dawley rats.

Sara Soleimani Asl, Kazem Mousavizadeh, Bagher Pourheydar, Mansoureh Soleimani, Elnaz Rahbar, Mehdi Mehdizadeh

Metabolic Brain Disease December 2013 DOI: 10.1007/s11011-013-9423-1 (opens in new tab)

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AI-extracted from the abstract
Characteristics Controlled animal experiment Peer reviewed
Sample size 56
Population Male Sprague Dawley rats weighing 200-250 g
Interventions MDMA N-acetyl-L-cysteine (NAC)
Dose 5, 10 or 20 mg/kg MDMA; NAC 100 mg/kg
Duration Twice daily injections; duration not stated
Measures Morris water maze (MWM), rectal temperature, hippocampal cell counts, Bcl-2, Bax, caspase-3 expression
Topics MDMA
Key findings NAC pretreatment significantly reduced MDMA-induced hyperthermia, attenuated the MDMA-induced increase in distance traveled and the decrease in time spent in the target quadrant in the Morris water maze, and protected against hippocampal cell death and changes in Bax, caspase-3, and Bcl-2 expression. The authors suggest a possible benefit of NAC for treating neurotoxicity among people who use MDMA.

Abstract

Exposure to 3, 4-methylenedioxymethamphetamine (MDMA) leads to spatial memory impairment and hippocampal cell death. In the present study we have examined the protective effects of N-acetyl-L-cysteine (NAC) on MDMA-induced neurotoxicity. A total of 56 male Sprague Dawley rats (200-250 g) received twice daily intraperitoneal (IP) injections of 5, 10 or 20 mg/kg MDMA plus NAC (100 mg/kg). Rectal temperatures were recorded before and after daily treatment. We used a Morris water maze (MWM) to assess spatial learning and memory. At the end of the study rats' brains were removed, cells were counted and the level of Bcl-2, Bax and caspase-3 expression in the hippocampi were measured. NAC pretreatment significantly reduced MDMA-induced hyperthermia. In the MWM, NAC significantly attenuated the MDMA-induced increase in distance traveled; however the observed increase in escape latency was not significant. The decrease in time spent in the target quadrant in MDMA animals was significantly attenuated (p < 0.001, all groups). NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2. This data suggested a possible benefit of NAC in the treatment of neurotoxicity among those who use MDMA.

Comparable studies

Other preclinical and animal studies on MDMA, most cited first.

Study Year Design Participants
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Rats (implied by typical neurochemical study context) 1987 Experimental study
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Rat brain 1987 Animal experiment
Comparison of the monoamine transporters from human and mouse in their sensitivities to psychostimulant drugs Human and mouse dopamine, norepinephrine, and serotonin transporters expressed in cells 2006 In vitro laboratory study
Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Rats 1998 Experimental study
Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Squirrel monkeys treated with MDMA 1999 Observational cohort

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