The effects of certain gasotransmitters inhibition on homocysteine acutely induced changes on rat cardiac acetylcholinesterase activity

Abstract

Background/Aim: Hyperhomocysteinaemia is linked to higher level of acetylcholinesterase (AChE) in brain, but there is insufficient information on influence of homocysteine (Hcy) and gasotransmitters on cardiac AChE. Thus, the aim of this study was to evaluate the influence of certain gasotransmitter inhibitors in Hcy-induced changes on rat cardiac AChE activity. Methods: Research was performed on 72 male Wistar albino rats distributed into 6 groups: 1) Control group-saline (1 ml 0.9 % NaCl ip); 2) DL-Hcy (8 mmol/kg ip DL homocysteine (DL-Hcy); 3) L-NAME (10 mg/kg ip N ω-Nitro-L-arginine methyl ester (L-NAME), inhibitor of NO production); 4) DL-PAG (50 mg/kg ip DL-propargylglycine (DL-PAG), inhibitor of H2S production); 5) DL-Hcy+L-NAME (8 mmol/ kg ip DL-Hcy + 10 mg/kg ip L-NAME); and 6) DL-Hcy+DL-PAG (8 mmol/kg ip DL-Hcy + 50 mg/kg ip DL-PAG). All tested substances were administered in a single dose, intraperitoneally, 60 minutes before animals' sacrifice. AChE activity was measured in the rats' cardiac tissue homogenate. Results: Administration of Hcy and L-NAME induced significant decrease in AChE activity compared with control condition. Administration of DL-PAG, DL-Hcy+L-NAME and DL-Hcy+DL-PAG did not change AChE activity compared with the control group. Conclusion: The effects of acute Hcy administration on the cardiac AChE activity are partially mediated via interaction with tested gasotransmitters.

Homocysteine, Vitamins B6 and Folic Acid in Experimental Models of Myocardial Infarction and Heart Failure—How Strong Is That Link?

“…HHcy also alters the bone microarchitecture and increases the risk of bone fracture [44]. An experimental study showed that Hcy can reduce the activity of cardiac acetylcholinesterase and alter heart function [45].…”