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- W2043008718 abstract "The role of oxygen in the induction of cellular damages during re-oxygenation of hypoxic hearts was studied in isolated Langendorff perfused rat hearts. An increase in the period of hypoxia of up to 80 min resulted in a decrease in both superoxide dismutase and glutathione peroxidase activity. This decrease continued when the hearts perfused in hypoxia for periods of 40 and 60 min were re-oxygenated for an additional 20 min. Under these conditions, re-oxygenation caused an increase in lipid peroxidation which was evaluated as malondialdehyde formation. In comparison to aerobic hearts, the cellular contents of acid soluble thiol groups, insoluble thiol groups and reduced glutathione were all decreased by hypoxia, while oxidized glutathione remained unchanged. The re-admission of oxygen to hypoxic hearts produced a further reduction in thiol groups and reduced glutathione. In contrast to well-oxygenated rat hearts, perfusion with substrate-free hypoxic medium resulted in a marked release of reduced glutathione into coronary effluents, which also continued after re-oxygenation. In hypoxia the release of oxidized glutathione began after 30 min of perfusion and slightly increased during the next 60 min of hypoxia. Re-oxygenation after 60 min of hypoxia did not enhance hypoxic oxidized glutathione release. These results suggest that re-oxygenation is able to induce lipid peroxidative damage in cardiac rat tissue when hypoxic substrate-free perfusions had previously reduced the cellular defensive mechanisms capable of neutralizing the toxic reactions mediated by oxygen metabolites." @default.
- W2043008718 created "2016-06-24" @default.
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- W2043008718 date "1980-08-01" @default.
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- W2043008718 title "Role of oxygen in the cellular damage induced by re-oxygenation of hypoxic heart" @default.
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- W2043008718 doi "https://doi.org/10.1016/0022-2828(80)90081-4" @default.
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