| Abstrakt: |
Release of enzymes from cytoplasmic and mitochondrial compartments was studied in rat heart cell cultures during and after 1 to 13 h of anoxia. From the cytoplasm, both α-hydroxy-butyrate dehydrogenase (HBDH) and cAST (the cytoplasmic isoenzyme of aspartate aminotransferase (AST)) are released in about equal proportions, reaching levels of about 80% of the original intracellular HBDH and cAST activities after 13 h of anoxia. From the mitochondria, mAST (the mitochondrial isoenzyme of AST) is released with some retardation compared with cAST, reaching levels of 34% of the original intracellular mAST activity after 13 h of anoxia. In contrast to anoxia, reoxygenation induces a rapid release of both mAST and cAST. The activity ratio mAST /total AST in the extracellular fluid varied from 0.06 ± 0.05 (mean ± SEM; n = 4) after 2 h of anoxia to 0.59 ± 0.02 (n = 4) after 10 h of anoxia. This ratio was 0.44 ± 0.07 (n = 4) after 2 h anoxia + 2 h reoxygenation, and 0.59 ± 0.02 (n = 4) after 10 h anoxia + 2 h reoxygenation, and this implies that, after reoxygenation, mAST/total AST is more or less independent of the duration of anoxia.In plasma of patients with acute myocardial infarction, obtained 24 h after onset of infarction, mAST/total AST ratio is low (0.13 ± 0.02, n = 12) at low total AST activities (≤ 80 U litre−1) and significantly (P < 0.01) higher (0.27 ± 0.05, n = 7) at AST activities exceeding 80 U litre−1.In contrast, mAST/total AST ratio in plasma of patients who underwent cardiac surgery, obtained 24 h after onset of cardiac surgery, is high (0.23 ± 0.02, n = 31) at low total AST activities (≤ 80 U litre−1).After comparison of the results obtained with heart cell cultures with those obtained in plasma of patients, this study gives evidence to the hypothesis that reoxygenation or reperfusion leads to oxygen-induced mitochondrial damage (oxygen-paradox) as reflected by a rapid release of considerable amounts of mAST. [ABSTRACT FROM PUBLISHER] |
