Abstract
1. Inhibitors of nitric oxide (NO) formation or ADP-ribosylation attenuate methamphetamine (METH)- and methylenedioxymetamphetamine (MDMA)-induced neurotoxicity on dopaminergic and serotonergic cells in primary cultures. 2. They also prevent METH-induced reactive gliosis in dopaminergic cultures. 3. Overexpression of superoxide dismutase (SOD) in cells obtained from SOD-transgenic mice also attenuates drug-induced toxicity. 4. These data indicate a role for oxygen-based and NO free radicals in the mechanisms of cell death associated with drugs of abuse in vitro.
MeSH terms
-
Adenosine Diphosphate Ribose / antagonists & inhibitors
-
Adenosine Diphosphate Ribose / metabolism*
-
Animals
-
Arginine / metabolism*
-
Brain / cytology
-
Brain / drug effects
-
Brain / embryology
-
Cell Death / drug effects
-
Cells, Cultured
-
Dopamine / metabolism
-
Dopamine Agents / toxicity
-
Female
-
Free Radicals
-
Gene Expression Regulation / drug effects
-
Gene Expression Regulation / genetics
-
Gliosis / prevention & control
-
Illicit Drugs / toxicity*
-
Methamphetamine / toxicity
-
Mice
-
Mice, Transgenic
-
N-Methyl-3,4-methylenedioxyamphetamine / toxicity
-
Nitric Oxide / antagonists & inhibitors
-
Nitric Oxide / metabolism*
-
Oxidative Stress / physiology*
-
Pregnancy
-
Serotonin / metabolism
-
Serotonin Agents / toxicity
-
Superoxide Dismutase / genetics
-
Superoxide Dismutase / metabolism
Substances
-
Dopamine Agents
-
Free Radicals
-
Illicit Drugs
-
Serotonin Agents
-
Adenosine Diphosphate Ribose
-
Nitric Oxide
-
Serotonin
-
Methamphetamine
-
Arginine
-
Superoxide Dismutase
-
N-Methyl-3,4-methylenedioxyamphetamine
-
Dopamine