Exercise causes oxidative damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls
| Autor: | Shailesh U. Rajguru, George S Yeargans, Norbert W. Seidler |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Male
medicine.medical_specialty Erythrocytes Physical Exertion Phospholipid Protein oxidation General Biochemistry Genetics and Molecular Biology Rats Sprague-Dawley Lipid peroxidation chemistry.chemical_compound Microsomes Internal medicine Blood plasma medicine Animals Sulfhydryl Compounds General Pharmacology Toxicology and Pharmaceutics Membranes Chemistry Muscles Myocardium Erythrocyte Membrane Cardiac muscle Skeletal muscle Heart General Medicine Malondialdehyde Rats Endocrinology medicine.anatomical_structure Biochemistry medicine.symptom Reactive Oxygen Species Oxidation-Reduction Muscle contraction |
| Zdroj: | Life Sciences. 54:149-157 |
| ISSN: | 0024-3205 |
| Popis: | The physiological and biochemical demands on contracting muscle make this tissue particularly susceptible to molecular and cellular damage. We looked at membrane structures in cardiac and skeletal muscle and in erythrocytes for exercise-induced lipid peroxidation. These tissues were removed from each of the rats used in this study. We also examined and compared the effects of exercise on the redox status of blood plasma, erythrocytes and cardiac and skeletal muscle from the same rats. We used a swim stress protocol to exercise the rats to exhaustion. Some form of chemical modification or oxidative damage to membranes was observed in all of the tissues tested. Cardiac muscle microsomes from exercised rats exhibited increased malondialdehyde and decreased phospholipid (control, 249.1 vs exercised, 120.6 nmols phospholipid/mg protein). Skeletal muscle microsomes showed decreased sulfhydryls, decreased phospholipid (control, 1,276.9 vs exercised, 137.7 nmols phospholipid/mg protein), increased malondialdehyde and greater protein crosslinking after exercise. Erythrocyte membranes also exhibited exercised-induced protein oxidation. However, the total cellular sulfhydryl content remained the same in erythrocytes and cardiac tissue but increased in blood plasma (control, 10.8 vs exercised, 24.7 μmols SH/dl plasma) and skeletal muscle after exercise. We conclude that exercise profoundly effects membrane structures. The body compensates for this lipid peroxidation and protein damage by increasing total cellular sulfhydryls in blood plasma and skeletal muscle which would aid in repair of the damaged membranes. |
| Databáze: | OpenAIRE |
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