title: Myocardial glutathione metabolic status in fat-fed rabbits.
abstract: Short-term fat feeding could exert adverse cardiac effects by altering myocardial glutathione-related antioxidant defenses. We have here assessed total glutathione (TG), the activities of glutathione reductase (GSSG-Red), γ-glutamylcysteine synthetase (γ-GCS), γ-glutamyl transpeptidase (γ-GT) and glutathione peroxidase (GSH-Px), fluorescent damage products of lipid peroxidation (FDPL), thiobarbituric acid-reactive substances (TBARS), H2O2, and ATP in the aerobically perfused hearts of control rabbits and of rabbits fed a fat-enriched diet for 18 days. Such biochemical parameters, myocardial hemodynamics and infarct size were assessed in the perfused hearts of other control and fat-fed rabbits subjected to 60 min global ischemia plus 30 min reperfusion. Compared to controls, a reduced activity of GSSG-Red and γ-GT associated with decreased TG content was detected in the aerobically perfused hearts of fat-fed rabbits, which also showed insignificant γ-GCS activation, GSH-Px depressed activity, FDPL, TBARS and H2O2 burden, and unaltered ATP content. Ischemia-reperfusion decreased the myocardial levels of TG, ATP, and γ-GCS activity and augmented those of FDPL, TBARS, and H2O2 especially in the fat-fed rabbits, without significant changes in myocardial GSSG-Red, γ-GT, and GSH-Px activities. Ischemia-reperfusion induced greater hemodynamic dysfunction and infarct size in the hearts of fat-fed rabbits than in those of controls. Thus, short-term fat feeding and hyperlipidemia alter glutathione metabolic status of the rabbit myocardium, inducing a GSSG-Red- and γ-GT-related decrement of myocardial glutathione content, which, together with GSH-Px dysfunction, may favor tissue oxidative stress and render the myocardium more susceptible to ischemia-reperfusion injury.
authors: Dipartimento di Medicina e Scienze dell'Invecchiamento, and Centro di Scienze dell'Invecchiamento-Fondazione Università G. d'Annunzio, Facoltà di Medicina e Chirurgia, Università "G. d'Annunzio", 66100, Chieti, Italy, dlapenna@unich.it.
authors: Domenico
authors: D
authors: Lapenna
authors: Giuliano
authors: G
authors: Ciofani
authors: Chiara
authors: C
authors: Cuccurullo
authors: Maria Adele
authors: MA
authors: Giamberardino
authors: Franco
authors: F
authors: Cuccurullo
mesh_terms: D000818:Animals; D059305:Diet, High-Fat; D005978:Glutathione / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism*; D005980:Glutathione Reductase / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000235:genetics; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000235:genetics; D011817:Rabbits; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism* / Q000473:pathology
chemical_list: D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005978:Glutathione