Circulation Research, Vol 61, 604-607, Copyright © 1987 by American Heart Association
ARTICLES |
B Schoutsen and JW de Jong
Cardiochemical Laboratory, Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
Myocardial xanthine oxidase has been associated with reoxygenation injury induced by oxygen radicals. The damage due to myocardial ischemia and reperfusion increases with age; therefore, one would expect to find more xanthine oxidase in adult than in young hearts. Consequently, we studied the age-dependence of xanthine oxidoreductase activity in hearts, in addition to the localization of the enzyme in cultured rat-heart cells. We measured xanthine oxidase plus dehydrogenase activity in homogenates of hearts and in homogenates of cultured neonatal myocytes and nonmuscular cells. In rat heart homogenates, xanthine oxidoreductase increased from 0.5 +/- 0.1 mU/g wet wt (newborn, mean +/- SD) to 25 +/- 4 mU/g (age 15 weeks, p less than 0.001). The value for adult rabbit heart was more than 1,000 times lower and hardly detectable. Therefore, we did not study young rabbit hearts. In rat myocyte cultures, xanthine oxidoreductase activity increased from 4.2 +/- 1.6 mU/g protein (2nd day of culture) to 17 +/- 4 mU/g (4th day, p less than 0.005). The activity in nonmuscular cells increased much more, from 10.1 +/- 1.1 to 117 +/- 25 mU/g (p less than 0.002). The age-related increase of xanthine oxidoreductase activity in rat heart is in agreement with the implied role in reperfusion damage by the enzyme. Whether myocytes, in which the enzyme has a low activity, could be damaged in this way, remains to be studied.
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