Volume 5, Number 4
+ Volume 5, 2017
Issue 1
Issue 2
Issue 3
Issue 4
+ Volume 4, 2016
+ Volume 3, 2015
+ Volume 2, 2014
+ Volume 1, 2013
Science International Vol. 5 (4), 2017
Research Article
Acetylcholinesterase as a Biomarker of Arsenic Induced Cardiotoxicity in Mammals
Vivek Kumar Gupta , Abhishek Kumar , Sarita H. Yadav , Rashmi Pandey and Bechan Sharma
Abstract: Background and Objective: Arsenic is an environmental toxicant and it exerts its toxic effect through the inhibition of various enzymes. The toxicity of arsenic results due to its ability to interact with sulfhydryl groups of proteins and enzymes and to substitute phosphorus in various biochemical reactions. The main objective of this study was to determine the effect of arsenic trioxide on the activity of acetylcholinesterase. In present article, the endeavor has been made in order to assess the arsenic mediated cardiotoxicity in vitro by assaying the activity of AChE from the post nuclear supernatant (PNS) of rat heart treated in the presence of different concentrations of arsenic. Materials and Methods: The rat homogenate heart tissue (10% w/v) was made in sodium phosphate buffer (50 mM; pH 7.4) containing Triton X-100 (0.2% v/v) and another that did not contain detergent using Potter-Elvehjam homogenizer fitted with teflon coated pestle under the ice-cold condition. The post nuclear supernatant of rat heart tissue was prepared by homogenizing the tissue followed by the centrifugation of tissue homogenate at 9000 rpm for 30 min using Sigma 2-16KL refrigerated centrifuge at 4°C. Statistical analysis of the data was performed using GraphPad Prism and chi-square goodness of fit test. Results: The experimental findings indicated that the enzyme was localized in the membrane bound fraction and could be solubilized by using 0.2% Triton X-100. The enzyme was found to be stable up to 30 days when stored at -20°C in phosphate buffer (50 mM, pH 7.4) containing 0.2% Triton X-100. The AChE exhibited Km, Vmax, Kcat, catalytic efficiency and IC50 values computed to be 0.1287 mM, 0.073 mM sec–1, 0.0017 sec–1, 0.0160 mM–1sec–1 and 1.14 mM, respectively. Conclusion: Taken together, these results indicated that AChE from rat heart could be exploited as a biomarker of arsenic induced cardiotoxicity.
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