Key result
In isolated rat hearts, the ESR sextet signal and cytosolic iron release occur simultaneously during post-ischaemic reperfusion, and the signal can be inhibited by the iron chelator desferrioxamine.
Why the study?
Does desferrioxamine inhibit the sextet signal observed during post-ischaemic reperfusion in isolated rat hearts?
Does desferrioxamine inhibit the sextet signal observed during post-ischaemic reperfusion in isolated rat hearts?
The sextet signal observed in spin-trapping experiments during post-ischaemic reperfusion is likely an artifact caused by catalytic activity of released non-protein bound cytosolic iron.
Suggests iron chelation for reperfusion injury; hypothesis-generating in rat models, human trials needed.
Previous studies of oxygen-derived free radical generation based on spin-trapping methods have shown a signal formed of six bands (sextet) using electron spin resonance spectrometry (ESR) of coronary effluents collected during post-ischaemic reperfusion of isolated hearts perfused with 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The origin of this signal has recently become controversial. In the present study we show that, in the rat, this sextet and cytosolic iron release occur simultaneously, and that this signal can be inhibited by the iron chelator desferrioxamine. It also appears that the iron release is not protein bound, and could therefore have a marked catalytic activity. This may be responsible for the production of an artefactural signal observed as the sextet.
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Boucher et al. (1992) studied Post-ischaemic reperfusion. Desferrioxamine was evaluated on ESR sextet signal and cytosolic iron release. In isolated rat hearts, the ESR sextet signal and cytosolic iron release occur simultaneously during post-ischaemic reperfusion, and the signal can be inhibited by the iron chelator desferrioxamine.
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