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• W2767428806 abstract "1. Mephedrone, a new and popular amphetamine drug, is widely abused and is still legal in some parts around the world. Little data on mechanisms involved in mephedrone induced cardiotoxicity are available. 2. Therefore, we decided to explain the mechanisms of mephedrone cardiotoxicity by using mitochondria isolated from rat heart. The isolated heart mitochondria were incubated with different concentrations of mephedrone (5, 10 and 20 µM). 3. Results showed that mephedrone induced mitochondrial dysfunction via an increase in mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling and damage in the mitochondrial outer membrane (MOM) which is associated with the cytochrome c release. Our results showed that decrease of ATP levels is an indicator of disturbance in oxidative phosphorylation. Also, mephedrone increased the caspase-3 activity. 4. According to the results, we suggest that mephedrone induced cardiotoxicity is the result of a disruptive effect on the mitochondrial respiratory chain and induction of ROS-mediated apoptosis signaling in heart cardiomyocytes." @default.
• W2767428806 created "2017-11-17" @default.
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• W2767428806 date "2017-11-28" @default.
• W2767428806 modified "2023-09-25" @default.
• W2767428806 title "Toxicity of new synthetic amphetamine drug mephedrone On Rat Heart mitochondria: a warning for its abuse" @default.
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• W2767428806 doi "https://doi.org/10.1080/00498254.2017.1401753" @default.
• W2767428806 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29105555" @default.
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