Guanidino compounds inhibit acetylcholinesterase and butyrylcholinesterase activities: Effect neuroprotector of vitamins E plus C

Abstract

Hyperargininemia is a metabolic disorder biochemically characterized by tissue accumulating of arginine and other guanidino compounds. Convulsions, lethargy and psychomotor delay or cognitive deterioration are predominant clinical features of this disease. Although neurologic symptoms predominate in this disorder, their pathophysiology is still unknown. In the present study we initially investigated the in vitro effect of arginine, homoarginine, N-acetylarginine and argininic acid on acetylcholinesterase and butyrylcholinesterase in hippocampus and serum of 15-, 30- and 60-day-old rats. Results showed that arginine in vitro significantly decreased acetylcholinesterase activity in hippocampus of 15-day-old rats and increased this enzyme activity in hippocampus of 60-day-old rats, homoarginine and N-acetylarginine significantly increased acetylcholinesterase activity both in hippocampus of 15- and 30-day-old rats. On the other hand, butyrylcholinesterase was inhibited by homoarginine in serum of 15-day-old rats. The influence of the antioxidants trolox and ascorbic acid on the effects elicited by arginine, homoarginine and N-acetylarginine was also studied. Results showed that these antioxidants were able to prevent the alteration on acetylcholinesterase and butyrylcholinesterase activities caused by guanidine compounds studied, suggesting that alterations on these cholinesterases were probably mediated by free radicals. It is presumed that these results might be associated, at least in part, with the neuronal dysfunction of patients affected by hyperargininemia.

Protective effects of vitamin E and selenium against dimethoate-induced cardiotoxicityin vivo: Biochemical and histological studies

“…These elements probably protected AchE activities via their antioxidant properties. Our hypothesis is in agreement with the study of Delwing‐de Lima et al () that has shown that antioxidants, like vitamins C and E, are able to prevent acetylcholinesterase alteration.…”

Oxidative stress and thyroid impairment after gibberellic acid treatment in pregnant and lactating rats and their offspring

“…Recent evidence suggests that besides AChE, BuChE catalyses the hydrolysis of the neurotransmitter, acetylcholine, and serves as a coregulator of cholinergic transmission [48]. During our experimental study, AChE and BuChE decreased in GA 3 group, suggesting the production of oxidative stress as reported by us and by others [49]. The decrease of AChE enzyme activity might be due, according to Das and Mukherjee [50], directly to pollutant effects on the active part of enzyme or indirectly to the inhibition of enzyme synthesis.…”

Impacts of oxidative stress on acetylcholinesterase transcription, and activity in embryos of zebrafish (Danio rerio) following Chlorpyrifos exposure

“…Neuroprotective effects of VC were previously observed through an increase of ChE activity in organisms exposed to anti-AChE chemicals (Bano and Bhatt, 2010;Delwing-de Lima et al, 2010). Similarly, VC was protective against CPF induced oxidative stress in tilapia (Özkan et al, 2012).…”