| First Author | Jayanthi S | Year | 1999 |
| Journal | Neuroscience | Volume | 91 |
| Issue | 4 | Pages | 1379-87 |
| PubMed ID | 10391444 | Mgi Jnum | J:57353 |
| Mgi Id | MGI:1344490 | Doi | 10.1016/s0306-4522(98)00698-8 |
| Citation | Jayanthi S, et al. (1999) Overexpression of human copper/zinc superoxide dismutase in transgenic mice attenuates oxidative stress caused by methylenedioxymethamphetamine (Ecstasy). Neuroscience 91(4):1379-87 |
| abstractText | Administration of 3,4-methylenedioxymethamphetamine (4 x 20 mg/kg) to non-transgenic CD-1 mice caused marked depletion in dopamine, 3,4- dihydroxyphenylacetic acid and 5-hydroxytryptamine in the caudate- putamen. There were no significant changes in serotonergic markers in the hippocampus and frontal cortex. Homozygous and heterozygous copper/zinc superoxide dismutase transgenic mice show partial protection against the toxic effects of 3,4- methylenedioxymethamphetamine on striatal dopaminergic markers. In addition, 3,4-methylenedioxymethamphetamine injections caused marked decreases in copper/zinc superoxide dismutase activity in the frontal cortex, caudate-putamen and hippocampus of wild-type mice. Moreover, there were concomitant 3,4-methylenedioxymethamphetamine-induced decreases in catalase activity in the caudate-putamen and hippocampus, decreases in glutathione peroxidase activity in the frontal cortex as well as increases in lipid peroxidation in the frontal cortex, caudate- putamen, and hippocampus of wild-type mice. In contrast, administration of 3,4-methylenedioxymethamphetamine to homozygous superoxide dismutase transgenic mice caused no significant changes in antioxidant enzyme activities nor in lipid peroxidation. These results provide further substantiation of a role for oxygen-based radicals in 3,4- methylenedioxymethamphetamine-induced neurotoxicity. The present data also suggest that free radicals generated during 3,4- methylenedioxymethamphetamine administration may perturb antioxidant enzymes. Consequently, there might be further overproduction of free radicals with associated peroxidative damage to cell membranes and associated terminal degeneration. |
