Involvement of oxidative and L-arginine-NO pathways in the neurotoxicity of drugs of abuse in vitro.
C Cerruti, P Sheng, Bruce Ladenheim, C J Epstein, J L Cadet
Clinical and experimental pharmacology & physiology May 1995 DOI: 10.1111/j.1440-1681.1995.tb02025.x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | In vitro experimental study Peer reviewed |
|---|---|
| Population | Primary cultures of dopaminergic and serotonergic cells, including cells from SOD-transgenic mice |
| Key findings | Inhibiting nitric oxide formation or ADP-ribosylation attenuated METH- and MDMA-induced neurotoxicity in dopaminergic and serotonergic cell cultures, and also prevented METH-induced reactive gliosis. Overexpression of superoxide dismutase in cells from transgenic mice similarly reduced drug-induced toxicity. 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. |
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.
Citations in the library
Cited by 2
- A study of the mechanisms involved in the neurotoxic action of 3,4‐methylenedioxymethamphetamine (MDMA, ‘ecstasy’) on dopamine neurones in mouse brain British Journal of Pharmacology December 1, 2001
- 3,4-Methylenedioxymethamphetamine (MDMA) Abuse may Cause Oxidative Stress and Potential Free Radical Damage Free Radical Research 2003