首页> 美国卫生研究院文献>Journal of the Boston Society of Medical Sciences >Lysosomal alterations in hypoxic and reoxygenated hearts. II. Immunohistochemical and biochemical changes in cathepsin D.
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Lysosomal alterations in hypoxic and reoxygenated hearts. II. Immunohistochemical and biochemical changes in cathepsin D.

机译:缺氧和复氧心脏中的溶酶体改变。二。组织蛋白酶D的免疫组织化学和生化变化。

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摘要

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.
机译:大鼠和兔心脏的亚致死性缺氧损伤伴随组织蛋白酶D活性的生化重新分布,从微粒到组织匀浆的上清液部分,再氧化后可部分逆转。组织蛋白酶D的免疫荧光染色未能揭示酸性水解酶的主要解剖释放,直到出现坏死为止,这表明较早的生化重新分布主要是由于匀浆过程中溶酶体脆弱性增加所致,该酶在细胞内的大量扩散仅是由于不可逆转的损害而发生的。地点。缺氧会导致组织蛋白酶D染色的溶酶体和不染色的液泡增大,并且聚集。这些变化在可逆性受损心脏的再充氧和恢复过程中加剧,表明溶酶体-微血管装置可能在缺氧性损伤后的心肌修复中发挥作用。

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