Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.23.5 (
cathepsin D
)
4,130
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The present investigation deals with the in vivo effects of oxygen free radicals (OFRs) in the absence and presence of scavengers of OFRs (superoxide dismutase, SOD, and catalase) on the cardiac function and contractility and with the in vitro effects of exogenous OFRs and various pH and pO2 on the release of acid hydrolases from dog myocardial lysosomes. The hemodynamic measurements were made before and at various intervals after administration of OFRs for up to 2 h.
Xanthine
plus xanthine oxidase (X-XO) and opsonized zymosan were used to generate OFRs. Oxygen free radicals produced a decrease in the cardiac function and indices of myocardial contractility. SOD alone or in combination with catalase tended to protect the cardiac function against the deleterious effects of OFRs. There was about a threefold increase in the release of
cathepsin D
activity in vitro from the lysosomes in the preparations treated with X-XO as compared to those without such treatment. The presence of SOD prevented the release of
cathepsin D
from the lysosomes. The changes in pH (4.5, 5.5, 6.0, 6.5, 7.4, 8.0) alone did not cause any increase in the enzyme release. However, the presence of OFRs at each pH resulted in a similar increase (about threefold) in the release of
cathepsin D
. Similarly the changes in pO2 alone did not cause the release of
cathepsin D
, but there were marked increases in the release of
cathepsin D
at each pO2 in the presence of OFRs. These data indicate that it is the oxygen free radicals and not the alterations in pH or pO2 that are primarily responsible for the release of lysosomal hydrolases.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Oxygen free radicals and cardiac depression. 792 55
