N-acetylcysteine amide protects against methamphetamine-induced tissue damage in CD-1 mice

Human & Experimental Toxicology
Xinsheng ZhangNuran Ercal

Abstract

Methamphetamine (METH), a highly addictive drug used worldwide, induces oxidative stress in various animal organs, especially the brain. This study evaluated oxidative damage caused by METH to tissues in CD-1 mice and identified a therapeutic drug that could protect against METH-induced toxicity. Male CD-1 mice were pretreated with a novel thiol antioxidant, N-acetylcysteine amide (NACA, 250 mg/kg body weight) or saline. Following this, METH (10 mg/kg body weight) or saline intraperitoneal injections were administered every 2 h over an 8-h period. Animals were killed 24 h after the last exposure. NACA-treated animals exposed to METH experienced significantly lower oxidative stress in their kidneys, livers, and brains than the untreated group, as indicated by their levels of glutathione, malondialdehyde, and protein carbonyl and their catalase and glutathione peroxidase activity. This suggests that METH induces oxidative stress in various organs and that a combination of NACA as a neuro- or tissue-protective agent, in conjunction with current treatment, might effectively treat METH abusers.

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Citations

Jul 2, 2016·The Journal of Surgical Research·Serdar TurkyilmazCengiz Ercin
Feb 15, 2015·Brain Research·Yasaswi MaddiralaNuran Ercal
Jun 1, 2016·Drug and Alcohol Review·Rebecca McKetinMichael Berk
Mar 1, 2017·Archives of Pharmacal Research·Eun-Joo ShinHyoung-Chun Kim
Jul 22, 2021·Archives of Pharmacal Research·Eun-Joo ShinHyoung-Chun Kim
Jun 30, 2021·Experimental Neurology·Subramaniam JayanthiJean Lud Cadet

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