No evidence of malonyldialdehyde formation during reoxygenation injury in vitamin E-deficient rat heart
| Autor: | Roger J. Willis, C. T. Marchant, Lindsay R. Jordan, D. M. Barron, S. M. Wilson |
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| Rok vydání: | 1993 |
| Předmět: |
Vitamin
Male medicine.medical_specialty Antioxidant Physiology medicine.medical_treatment Ischemia Myocardial Reperfusion Myocardial Reperfusion Injury In Vitro Techniques Lipid peroxidation chemistry.chemical_compound Physiology (medical) Internal medicine Malondialdehyde medicine Animals Vitamin E Vitamin E Deficiency Rats Wistar Creatine Kinase biology business.industry Myocardium medicine.disease Rats Perfusion Endocrinology Biochemistry chemistry biology.protein Creatine kinase Vitamin E deficiency Cardiology and Cardiovascular Medicine business |
| Zdroj: | Basic research in cardiology. 88(4) |
| ISSN: | 0300-8428 |
| Popis: | Vitamin E is an endogenous antioxidant and is known to afford protection against lipid peroxidation. If lipid peroxidation was an important factor in the pathogenesis of reoxygenation injury in heart, then both the extent of lipid peroxidation and cell injury would be expected to be exacerbated in vitamin E-deficient hearts. To study reoxygenation injury in the present experiments, rat hearts were perfused in the Langendorff mode with a modified Krebs-Henseleit buffer under anoxic conditions for 60 min before resuming normoxic perfusion for 20 min. Creatine phosphokinase (CPK) activity and malonyldialdehyde (MDA), a product of lipid peroxidation, were assayed in the perfusate effluent from hearts during reoxygenation injury. Also, myocardial MDA and vitamin E contents were measured in extracts of freeze-clamped heart tissue obtained immediately before and 2 min after reoxygenation. Experiments were performed on hearts from groups of weanling rats fed either a vitamin E-deficient or vitamin E-supplemented diet (50 I.U. vitamin E/kg) for 5 to 6 weeks. After 5 weeks, the myocardial vitamin-E content was 103.8±5.3 (n=5) and 11.5±1.6 (n=4) ng/mg protein (mean±SEM) in the vitamin E-supplemented and vitamin E-deficient groups respectively. Perfused hearts from both dietary groups showed a peak of enzyme release 2 to 3 min after the reintroduction of oxygen, and enzyme release from vitamin E-deficient hearts was two-fold greater than enzyme release from vitamin E-supplemented hearts. MDA was not detected in the effluent perfusate of either group of hearts ( |
| Databáze: | OpenAIRE |
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