Arginine Administration Decreases Cerebral Cortex Acetylcholinesterase and Serum Butyrylcholinesterase Probably by Oxidative Stress Induction

Abstract

In the present study we investigated the action of vitamins E and C on the inhibition of acetylcholinesterase and butyrylcholinesterase activities provoked by arginine in cerebral cortex and serum of 60-day-old rats. Animals were pretreated for 1 week with daily intraperitoneal administration of saline (control) or vitamins E (40 mg/kg) and C (100 mg/kg). Twelve hours after the last injection, animals received one injection of arginine (0.8 microM/g of body weight) or saline. Results showed that acetylcholinesterase and butyrylcholinesterase activities were decreased in the arginine-treated rats. Furthermore, pretreatment with vitamins E and C prevented these effects. The data indicate that the reduction of acetylcholinesterase and butyrylcholinesterase activities caused by arginine was probably mediated by oxidative stress. Assuming the possibility that these effects might also occur in the human condition, our findings may be relevant to explain, at least in part, the neurological dysfunction associated with hyperargininemia and might support a novel therapeutic strategy to slow the progression of neurodegeneration in this disorder.

The effect of bisphenol A on some oxidative stress parameters and acetylcholinesterase activity in the heart of male albino rats

“…Very few evidences suggest that inhibition of AchE is mediated by oxidative stress (Wyse et al 2004). This was supported by the notion that hydroxyl radicals are involved in the AchE inhibition (Tsakiris et al 2000).…”

Effects of hexachlorobenzene on antioxidant status of liver and brain of common carp (Cyprinus carpio)

“…For instance, the AChE deactivation in rat erythrocytes by pyrethroid was correlated with the LPO status (Kale et al, 1999). Moreover, AChE inhibition in the arginine-treated rats could be prevented by the pretreatment with vitamins E and C (Wyse et al, 2004). In the present study, dose-dependent inhibition of AchE activity (R = À0.817, P = 0.047) was found and the parameter had good correlations to GSH (R = 0.903, P = 0.013) and SOD (R = 0.891, P = 0.017).…”

Hyperargininemia due to arginase I deficiency: the original patients and their natural history, and a review of the literature

“…NO is an important modulator of neuronal function (Prast and Philippu 2001). At pathological levels, it adversely affects brain function by induction of oxidative stress (Wyse et al 2004) and may promote the development of neurodegenerative diseases (Virarkar et al 2013). l-Arginine is a substrate for NOS, and increased l-arginine levels have been associated with increased NO production (Buchmann et al 1996; Wu and Morris 1998).…”