Effect of Manganese on Enzymes in Rat Brain

Abstract

Rats were given MnCl2.4H2O (8 mg/kg) intraperitoneally daily for 120 days, and then sacrificed by decapitation. The brain was removed and dissected into three regions; cerebral cortex, cerebellum and remainder of the brain. Enzymic studies were conducted in these regions and compared with control animals. The activities of acetyl choline esterase and adenosine deaminase were significantly reduced in all the three regions. The activity of monoamine oxidase was increased in the cerebellum while the activity of guanine deaminase decreased in the cerebellum and remainder of the brain. The analysis of the results allows no overall generalization in enzymic alterations induced by manganese chloride in the three regions of the rat brain.

The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain

“…The results are contradictory to those of Liapi et al (2008) and in agreement with Deskin et al (1981), Lai et al (1981, 1982), Martinez and Bonilla (1981) and Sitaramayya et al (1974). Deskin et al (1981) reported that AChE activity was significantly reduced in the striatum of rats treated with MnCl 2 (20 μg/g body weight/day), administered by oral gavage from birth to day 24 post-partum .…”

“…Deskin et al (1981) reported that AChE activity was significantly reduced in the striatum of rats treated with MnCl 2 (20 μg/g body weight/day), administered by oral gavage from birth to day 24 post-partum . Sitaramayya et al (1974) reported a significant decrease of AChE activity in the cerebral cortex, cerebellum and the remaining cerebral tissue in rats treated with MnCl 2 inoculated intraperitoneally for 120 days. In contrast, Liapi et al (2008) reported a significant increase of the activity of AChE in rats’ whole brains treated daily with MnCl 2 50 mg/Kg for 7 days by the i.p.…”

“…Mn-induced cortical cholinergic dysfunction is compatible with these cognitive de cits, as well as with the dementia observed later on in the clinical course of manganism (Finkelstein et al, 2007). Significant inhibition of acetylcholinesterase (AChE) activity was observed following lengthy periods of exposure to Mn in adult (Sitaramayya et al, 1974; Martinez and Bonilla, 1981) and neonatal (Deskin et al, 1981; Lai et al, 1984) rat brain. The inhibition of AChE prevents the hydrolysis of acetylcholine (ACh), leading to accumulation of ACh in the synaptic cleft and overstimulation of muscarinic and nicotinic ACh receptors.…”