C. Coudray et al., EFFECT OF ISCHEMIA REPERFUSION SEQUENCE ON CYTOSOLIC IRON STATUS AND ITS RELEASE IN THE CORONARY EFFLUENT IN ISOLATED RAT HEARTS/, Biological trace element research, 41(1-2), 1994, pp. 69-75
The hypothesis that oxygen-derived free radicals play an important rol
e in myocardial ischemic and reperfusion injury has received a lot of
support. In the presence of catalytic amounts of transition metals suc
h as iron, superoxide anions, and hydrogen peroxide can be transformed
into a highly reactive hydroxyl radical degrees OH (Haber-Weiss react
ion). In view of this, we have undertaken this study to investigate wh
ether iron is involved in the reperfusion syndrome and therefore could
aggravate free radicals injury. Coronary effluent iron concentrations
and cardiac cytosolic iron levels were evaluated in rat hearts subjec
ted to an ischemia/reperfusion sequences. In the case of total ischemi
a, iron concentration in coronary effluents peaked immediately in the
first sample collected upon reperfusion. However, in the case of parti
al ischemia, iron concentration in coronary effluents peaked rather ex
clusively during ischemia period. Cardiac cytosolic iron level augment
ed significantly after 30 min of total ischemia and non significantly
in the other ischemia protocols compared to perfused control hearts. I
t also appears that the iron released is not protein-bound, and could
therefore have a marked catalytic activity. The results of the present
study suggest that in the oxygen paradox, iron plays an important rol
e in inducing alterations during reoxygenation.