文摘
Our previous findings revealed that increased oxidative stress, apoptosis and necrosis were implicated in acute fluoride (F−) induced cardiac dysfunction apart from hypocalcemia and hyperkalemia. Cardiac intermediate filaments (desmin and vimentin) and cytoskeleton linker molecule vinculin plays an imperative role in maintaining the architecture of cardiac cytoskeleton. In addition, AMPK is a stress activated kinase that regulates the energy homeostasis during stressed state. The present study was aimed to examine the role of cytoskeletal proteins and AMPK signaling molecules in acute F− induced cardiotoxicity in rats.MethodsIn order to study this, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F− for 24 h.ResultsAcute F− intoxicated rats showed declined cytoskeletal protein expression of desmin, vimentin and vinculin in a dose dependent manner compared to control. A significant increase in phosphorylation of AMPKα (Thr172), AMPKß1 (Ser108) and Acetyl-coA carboxylase (ACC) (Ser79) in the myocardium and associated ATP deprivation were found in acute F− intoxicated rats. Further, ultra-structural studies confirmed myofibril lysis with interruption of Z lines, dilated sarcoplasmic reticulum and damaged mitochondrion were observed in both the groups of F− intoxicated rats.ConclusionTaken together, these findings reveal that acute F− exposure causes sudden heart failure by altering the expression of cytoskeletal proteins and AMPK signaling molecules.
