Effect of dietary antioxidant trace element supply on cardiac tolerance to ischemia-reperfusion in the rat.
Over a 10-week period, female Wistar rats received a diet containing various levels of four trace elements (Zn, Cu, Mn, Se), co-factors of antioxidant enzymes (superoxide dismutase SOD, glutathione peroxidase GPx), in order to examine the influence of supplementation or deficiency of these elements (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 total global normothermic ischemia, followed by reperfusion. The effects of the various diets (deficient, standard or supplemented) were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDP, dP/dtmax, heart rate x LVDP) as well as ultrastructural tissue characteristics. Furthermore, SOD and GPx activities were measured before ischemia and at the end of the reperfusion period. Results suggest that: (a) the activity of antioxidant enzymes increased or decreased significantly when diet was respectively supplemented with, or deficient in, trace elements, but was not further modified by an ischemia-reperfusion episode: (b) the recovery of cardiac function during reperfusion, and ventricular myocardial ultrastructure were significantly improved under the influence of trace element supplementation when compared to both standard and deficient groups. These results illustrate the protective effect of trace elements which are co-factors of antioxidant enzymes in limiting ischemia-reperfusion induced injury, and suggest a possible use in the field of anti-ischemic therapy.
Pucheu
S
S
Groupe de Physiopathologie Cellulaire Cardiaque, URA CNRS 1287, Université Joseph Fourier, Grenoble, France.
Coudray
C
C
Tresallet
N
N
Favier
A
A
de Leiris
J
J
D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D003300:Copper / Q000008:administration & dosage / Q000172:deficiency / Q000627:therapeutic use; D004032:Diet; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006321:Heart / Q000187:drug effects*; D006352:Heart Ventricles / Q000737:chemistry / Q000648:ultrastructure; D008345:Manganese / Q000008:administration & dosage / Q000172:deficiency / Q000627:therapeutic use; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012643:Selenium / Q000008:administration & dosage / Q000172:deficiency / Q000627:therapeutic use; D013482:Superoxide Dismutase / Q000378:metabolism*; D014131:Trace Elements / Q000008:administration & dosage / Q000172:deficiency / Q000627:therapeutic use*; D015032:Zinc / Q000008:administration & dosage / Q000172:deficiency / Q000627:therapeutic use
D000975:Antioxidants; D017382:Reactive Oxygen Species; D014131:Trace Elements; D008345:Manganese; D003300:Copper; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium; D015032:Zinc