Abstract
The accumulation of the aldehydic lipid peroxidation product 4-hydroxynonenal and thiobarbituric acid-reactive substances was demonstrated during anoxia/reoxygenation of isolated rat hepatocytes. 4-Hydroxynonenal was detected as dinitrophenylhydrazone derivative by means of an isocratic HPLC separation. The highest 4-hydroxynonenal level was found 15 min after the beginning of reoxygenation. The concentration of 4-hydroxynonenal was compared with the thiobarbituric acid-reactive substances formation, the glutathione status, and the cell viability. Addition of the xanthine oxidase inhibitor oxypurinol decreased the aldehyde formation during the reoxygenation phase. The same suppression of oxidative load by 20 μM oxypurinol (inhibition of xanthine oxidase) and by 1 mM oxypurinol (inhibition of xanthine oxidase plus radical scavenging) leads to two conclusions: First, the purine degradation is the primary radical source of postanoxic hepatocytes; second, the inhibition of radical generation by xanthine oxidase is the main component of cell protecting by oxypurinol. On the other hand, oxypurinol addition did not accelerate the adenosine 5′-triphosphate (ATP) restoration.
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