These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: N-acetylcysteine prevents memory deficits, the decrease in acetylcholinesterase activity and oxidative stress in rats exposed to cadmium.
    Author: Gonçalves JF, Fiorenza AM, Spanevello RM, Mazzanti CM, Bochi GV, Antes FG, Stefanello N, Rubin MA, Dressler VL, Morsch VM, Schetinger MR.
    Journal: Chem Biol Interact; 2010 Jun 07; 186(1):53-60. PubMed ID: 20399762.
    Abstract:
    The present study investigated the effect of the administration of N-acetylcysteine (NAC), on memory, on acetylcholinesterase (AChE) activity and on lipid peroxidation in different brain structures in cadmium (Cd)-exposed rats. The rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. The animals were divided into four groups (n=12-13): control/saline, NAC, Cd, and Cd/NAC. The results showed a decrease in step-down latency in the Cd-group, but NAC reversed the impairment of memory induced by Cd intoxication. Rats exposed to Cd and/or treated with NAC did not demonstrate altered shock sensitivity. Decreased AChE activity was found in hippocampus, cerebellum and hypothalamus in the Cd-group but NAC reversed this effect totally or partially while in cortex synaptosomes and striatum there was no alteration in AChE activity. An increase in TBARS levels was found in hippocampus, cerebellum and hypothalamus in the Cd-group and NAC abolished this effect while in striatum there was no alteration in TBARS levels. Urea and creatinine levels were increased in serum of Cd-intoxicated rats, but NAC was able to abolish these undesirable effects. The present findings show that treatment with NAC prevented the Cd-mediated decrease in AChE activity, as well as oxidative stress and consequent memory impairment in Cd-exposed rats, demonstrating that this compound may modulate cholinergic neurotransmission and consequently improve cognition. However, it is necessary to note that the mild renal failure may be a contributor to the behavioral impairment found in this investigation.
    [Abstract] [Full Text] [Related] [New Search]