Abstract
The effects of oxygen-derived radical scavengers (ODRS) on the heart was investigated during the calcium paradox. Perfusion with Ca2 +-free medium caused cell separation at the intercalated discs and changes in the endothelial cells. Upon Ca2+ reintroduction, a massive cell damage occurred. The cytosolic enzyme, creatine phosphokinase (CPK), was released in large amounts (p< 0.001). The tissue adenosine triphosphate (ATP) was reduced to 3.7 μmol/g dry weight from the control value of 21.6 μmol/g dry weight and tissue Ca2+ content was increased threefold. The treatment with Superoxide dismutase (SOD) and catalase (CAT) increased percentage of normal cells (62.2%) compared to nontreated Ca2+ paradox group (0.2%) and caused negligible leakage of CPK. Tissue ATP was preserved (p<0.03), and Ca2+ content was also reduced in the hearts treated with SOD and CAT (p<0.03). The cell membranes and vascular endothelium were well preserved in the hearts treated with SOD and CAT. Boiled SOD and CAT administered were totally ineffective. It is suggested that oxygen-active species may have a role in the Ca2+ paradox injury.
Original language | English (US) |
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Pages (from-to) | 27-37 |
Number of pages | 11 |
Journal | Virchows Archiv B Cell Pathology Including Molecular Pathology |
Volume | 54 |
Issue number | 1 |
DOIs | |
State | Published - Dec 1987 |
Externally published | Yes |
Keywords
- ATP
- Ca
- Calcium paradox
- Catalase
- Cell membrane
- Cytochrome C
- Heart
- Oxygen derived radicals
- Superoxide anion
- Superoxide dismutase
- Vascular endothelium
ASJC Scopus subject areas
- Pathology and Forensic Medicine