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P3‐305: Possible role of N‐acetyl cysteine against aluminum‐induced cognitive dysfunction and oxidative damage in rats
Author(s) -
Kumar Anil
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.1747
Subject(s) - oxidative stress , morris water navigation task , neuroprotection , pharmacology , acetylcysteine , elevated plus maze , chemistry , cholinesterase , medicine , endocrinology , biochemistry , antioxidant , psychiatry , anxiety , hippocampal formation
Background: Aluminium is potent neurotoxins, involved in the initiation and progression of various cognitive disorders like Alzheimer’s disease. Prolonged aluminium exposure induces oxidative stress and increases amyloid beta levels in vivo. The role of oxidative stress has been well suggested in these cognitive problems. Therefore, the present study has been designed to explore the possible role N-acetyl cysteine (NAC) against aluminiummediating cognitive dysfunction and oxidative stress in rats. Methods: Aluminium chloride (100mg/kg, p.o.) was given to rats for 6 weeks daily. Rats were concomitantly treated with NAC (per se; 50 and 100 mg/kg, i.p.) daily for a period of 6 weeks. On the 3 (21 ) and 6 week (42 day) of the study, various behavioral test (Morris water maze and elevated plus maze task paradigms) and locomotion (photoactometer) were done to evaluate cognitive tasks. The rats were sacrificed on 43 day following the last behavioral test and various biochemical tests were performed to assess the extent of oxidative damage. Results: Chronic aluminium chloride administration resulted in poor retention of memory in Morris water maze, elevated plus maze task paradigms and causedmarked oxidative damage. It also caused a significant increase in the acetyl cholinesterase activity. Chronic administration of NAC significantly improved memory retention in tasks, attenuated oxidative damage and acetyl cholinesterase activity in aluminium treated rats. Conclusions: Study suggests the neuroprotective effect of NAC against aluminium-induced cognitive dysfunction and oxidative damage.