Lysosomal alterations in hypoxic and reoxygenated hearts. II. Immunohistochemical and biochemical changes in cathepsin D.
Sublethal hypoxic injury in rat and rabbit hearts was accompanied by a biochemical redistribution of cathepsin D activity from the particulate to the supernatant fraction of the tissue homogenate, which was partially reversible on reoxygenation. Immunofluorescent staining for cathepsin D failed to reveal major anatomic release of the acid hydrolase until necrosis was present, suggesting that the earlier biochemical redistribution was primarily a result of increased lysosomal fragility during homogenization, with significant intracellular diffusion of the enzyme occurring only as irreversible damage took place. Hypoxia produced enlargement of both cathepsin-D-staining lysosomes and nonstaining vacuoles, as well as their aggregation. These changes were intensified during reoxygenation and recovery of reversibly damaged hearts, suggesting a possible role for the lysosomal-vacuolar apparatus in myocytic repair following hypoxic injury.
D000818:Animals; D002403:Cathepsins / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005455:Fluorescent Antibody Technique; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D066298:In Vitro Techniques; D007511:Ischemia / Q000378:metabolism; D008247:Lysosomes / Q000201:enzymology* / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011817:Rabbits; D051381:Rats
D002403:Cathepsins