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All rights reserved.N-acetylcysteine has been shown to have a positive effect on the clinical course of COPD. It would be of great value in the health care field to develop drugs like NACA as more effective and safer options for the prevention and therapeutic intervention in APAP-induced toxicity.Īcetaminophen GSH-prodrug Glutathione Hepatotoxicity NAPQI Oxidative stress.Ĭopyright © 2015 Elsevier Ireland Ltd. Thus, NACA appears to be better than NAC in reducing the oxidative stress induced by APAP. However, at the dose used, NAC was not effective in combating the oxidative stress induced by APAP. NACA significantly increased GSH levels and the GSH/GSSG ratio in the liver to 66.5% and 60.5% of the control, respectively and it reduced the level of ALT by 30%. Our results showed that NACA is better than NAC at a low dose (106mg/kg) in preventing oxidative stress and protecting against APAP-induced damage. Therefore, we studied the protective effects of N-acetylcysteine amide (NACA), a novel antioxidant with higher bioavailability, and compared it with NAC in APAP-induced hepatotoxicity in C57BL/6 mice. administration of NAC in a hospital setting are laborious and costly. Unfortunately, fairly high doses and longer treatment times are required due to its poor bioavailability. N-acetylcysteine (NAC), a GSH precursor, is the only currently approved antidote for an acetaminophen overdose. Depletion of glutathione (GSH) is one of the initiating steps in APAP-induced hepatotoxicity therefore, one strategy for restricting organ damage is to restore GSH levels by using GSH prodrugs.

It is safe at therapeutic doses, but its overdose can result in severe hepatotoxicity, a leading cause of drug-induced acute liver failure in the USA. Acetaminophen (N-acetyl-p-aminophenol, APAP) is one of the most widely used over the counter antipyretic and analgesic medications.