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Oxygen free radicals and cardiac depression
1Department of Pathology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Clinical Biochemistry
|June 1, 1994
Summary
Oxygen free radicals (OFRs) impair cardiac function and increase lysosomal enzyme release. Antioxidants like superoxide dismutase (SOD) and catalase protect the heart from OFR damage, suggesting OFRs are key to lysosomal hydrolase release.
Area of Science:
- Cardiology
- Biochemistry
- Cell Biology
Background:
- Oxygen free radicals (OFRs) are implicated in cellular damage.
- Lysosomal hydrolases play a role in cellular function and pathology.
Purpose of the Study:
- To investigate the in vivo effects of OFRs on cardiac function.
- To examine the in vitro effects of OFRs on lysosomal enzyme release from dog myocardial lysosomes.
- To determine the role of pH and pO2 in OFR-induced lysosomal enzyme release.
Main Methods:
- Hemodynamic measurements in dogs before and after OFR administration.
- Generation of OFRs using xanthine plus xanthine oxidase (X-XO) and opsonized zymosan.
- In vitro assessment of cathepsin D release from myocardial lysosomes under varying pH and pO2 conditions, with and without OFR scavengers (SOD, catalase).
Main Results:
- OFRs significantly decreased cardiac function and contractility in vivo.
- Superoxide dismutase (SOD) and catalase provided protection against OFR-induced cardiac dysfunction.
- In vitro, OFRs caused a threefold increase in cathepsin D release from lysosomes, which was prevented by SOD.
- Altered pH or pO2 alone did not induce enzyme release, but OFRs caused significant release at all tested pH and pO2 levels.
Conclusions:
- Oxygen free radicals are primarily responsible for the release of lysosomal hydrolases.
- OFRs have deleterious effects on cardiac function.
- Antioxidant enzymes like SOD and catalase can mitigate the harmful effects of OFRs on the heart and lysosomes.