title: Caffeic acid attenuates malathion induced metabolic disruption in rat liver, involvement of acetylcholinesterase activity.
abstract: It has been confirmed that organophosphorus compounds OP altered glucose homeostasis. Considerable experimental and clinical evidences have contributed the beneficial effects of polyphenol molecules on metabolic homeostasis. However, up to date limited studies have been performed on this topic. The aim of this study was to evaluate whether caffeic acid, an active phenolic component was able to reduce metabolic disruption induced by malathion administration. Malathion at 100mg/kg was administered to rats alone or in combination with caffeic acid at100 mg/kg. Malathion decreases hepatic GP activity and increases HK activity accompanied with a rise in the hepatic glycogen rate. Moreover, coadministration of malathion with caffeic acid resulted in restoration of malathion-induced GP inhibition and HK1 increase. These results may be due to the significant increase recorded in acetylcholinesterase (AchE) activity in vivo after coadministration of malathion and caffeic acid. Indeed, malathion is known to inhibit AChE activity leads to subsequent activation of cholinergic receptor that increased in part, catecholamine and glucocorticoids secretion; provoked glycogenolysis and gluconeogenesis activation. Thus, we can suggest that increase's (AchE) activity seems to be responsible for caffeic acid restoration on malathion-induced metabolic disruptions. Recent studies support the hypothesis that oxons bind to a secondary site on acetylcholinesterase, leading to activation/inhibition of the catalytic site. Thus, caffeic acid or its derivates may be leading to activation of the catalytic site within the second site interaction.
authors.affiliation: Laboratoire de Physiologie des Agressions, Département de Biologie, Faculté des Sciences de Tunis, Campus Universitaire El-manar, 2092 Tunis, Tunisia. raja.rezg@laposte.net
authors.forename: Raja
authors.initials: R
authors.lastname: Rezg
authors.forename: Bessem
authors.initials: B
authors.lastname: Mornagui
authors.forename: Saloua
authors.initials: S
authors.lastname: El-Fazaa
authors.forename: Najoua
authors.initials: N
authors.lastname: Gharbi
mesh_terms: D000110:Acetylcholinesterase / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002109:Caffeic Acids / Q000494:pharmacology*; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D006003:Glycogen / Q000378:metabolism; D024981:Glycogen Phosphorylase / Q000187:drug effects / Q000378:metabolism; D006593:Hexokinase / Q000187:drug effects / Q000378:metabolism; D007306:Insecticides / Q000633:toxicity; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008294:Malathion / Q000633:toxicity*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D002109:Caffeic Acids; D002800:Cholinesterase Inhibitors; D007306:Insecticides; D006003:Glycogen; D024981:Glycogen Phosphorylase; D006593:Hexokinase; D000110:Acetylcholinesterase; C040048:caffeic acid; D008294:Malathion