Effects of selenium deficiency on the response of cardiac tissue to ischemia and reperfusion

Over a 10-week period, female Wistar rats received a diet containing a low level of selenium, cofactor of the antioxidant enzyme glutathione peroxidase (GPx) in order to examine the influence of deficiency of this trace element (i) on tissue antioxidant enzyme defence systems, and (ii) on the suscep...

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Veröffentlicht in:Toxicology (Amsterdam) 2000-08, Vol.148 (2), p.125-132
Hauptverfasser: Toufektsian, Marie-Claire, Boucher, François, Pucheu, Sylvie, Tanguy, Stéphane, Ribuot, Christophe, Sanou, Drissa, Tresallet, Nicole, de Leiris, Joël
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container_issue 2
container_start_page 125
container_title Toxicology (Amsterdam)
container_volume 148
creator Toufektsian, Marie-Claire
Boucher, François
Pucheu, Sylvie
Tanguy, Stéphane
Ribuot, Christophe
Sanou, Drissa
Tresallet, Nicole
de Leiris, Joël
description Over a 10-week period, female Wistar rats received a diet containing a low level of selenium, cofactor of the antioxidant enzyme glutathione peroxidase (GPx) in order to examine the influence of deficiency of this trace element (i) on tissue antioxidant enzyme defence systems, and (ii) on the susceptibility of the myocardium to ischemia-reperfusion injury. At the end of the dietary treatment, hearts were perfused at constant flow (11 ml/min) before being subjected to 15 min of global normothermic ischemia, followed by 30 min of reperfusion. The effects of selenium deficiency were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDevP, heart rate HR, and the product HR x LVDevP), as well as ultrastructural tissue characteristics. Furthermore, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured at the end of the reperfusion period. Results suggest that: (a) the activity of GPx is decreased by selenium deficiency while SOD activity remains unchanged, (b) the recovery of cardiac function and myocardial ventricular ultrastructure during reperfusion are altered in the selenium-deficient group compared to controls. These results illustrate the crucial role that selenium, the co-factor of one of the major antioxidant enzymes of the myocardium, plays in determining the vulnerability of the heart to ischemia and reperfusion.
doi_str_mv 10.1016/S0300-483X(00)00203-1
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subjects Animals
Biological and medical sciences
Cell metabolism, cell oxidation
Cell physiology
Female
Fundamental and applied biological sciences. Psychology
Glutathione peroxidase
Glutathione Peroxidase - metabolism
Heart - drug effects
Heart - physiopathology
Heart Rate - drug effects
Heart Ventricles - drug effects
Heart Ventricles - physiopathology
Heart Ventricles - ultrastructure
Isolated rat heart
Molecular and cellular biology
Myocardial Ischemia - complications
Myocardial Reperfusion Injury - etiology
Myocardial Reperfusion Injury - physiopathology
Myocardial Reperfusion Injury - prevention & control
Myocardium - cytology
Myocardium - enzymology
Rats
Rats, Wistar
Reperfusion
Selenium
Selenium - administration & dosage
Selenium - deficiency
Superoxide Dismutase - metabolism
title Effects of selenium deficiency on the response of cardiac tissue to ischemia and reperfusion
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