The present study was undertaken to determine whether significant breakdown
of adenine nucleotides to purine bases and oxypurines occurred in mitochondria following
myocardial ischemia and ischemia followed by reperfusion, and whether allopurinol prevented
this effect. The adenine nucleotides adenosine, hypoxanthine, xanthine and uric acid
were measured in the mitochondria and the results suggest that breakdown did occur. Malondialdehyde
concentration was determined to gauge lipid peroxidation. This substance did
not increase during ischemia or reperfusion, but did so in the presence of allopurinol. Xanthine
dehydrogenase was converted to xanthine oxidase during reperfusion and the activity
of both enzymes were inhibited by allopurinol. The results also suggested the presence of a
mitochondrial 5'-nucleotidase. We conclude that significant breakdown of adenine nucleotide
took place in myocardial mitochondria during ischemia and ischemia followed by reperfusion
and that allopurinol may have a protective effect.
Recent evidence suggests that free oxygen radicals are produced by ischaemic
tissues, accounting for at least part of the damage that results. These free oxygen radicals are
produced by xanthine oxidase, amongst others, and removed by scavenger enzymes (catalase,
superoxide dismutase and glutathione peroxidase) and anti-oxidants. As mitochondria
are oxygen-utilising organelles, they are capable of producing free oxygen radicals. Our
results indicate that the removal of free oxygen radicals are not diminished during ischaemia,
but the activity of the free oxygen radical generator, xanthine oxidase, is increased. This
could lead to an increased superoxide anion concentration.
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