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钙反常诱导后心脏溶酶体水解酶的变化

Alterations in cardiac lysosomal hydrolases following induction of the calcium paradox.

作者信息

Kutryk M J, Dhalla N S

机构信息

Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Man., Canada.

出版信息

Can J Physiol Pharmacol. 1987 Nov;65(11):2175-81. doi: 10.1139/y87-343.

Abstract

Although perfusion of the heart with calcium-free medium for a brief period followed by reperfusion with calcium-containing medium results in marked structural derangements (calcium paradox), the mechanisms for this cell damage are far from clear. Since activation of lysosomal enzymes has been associated with pathological damage, it was the purpose of this study to examine alterations in the activities of several lysosomal enzymes in rat hearts subjected to calcium paradox. No significant changes in the activities of beta-acetylglucosaminidase, beta-galactosidase, alpha-mannosidase, or acid phosphatase were seen in the homogenates of hearts exposed to the calcium paradox. However, there were dramatic alterations in the lysosomal enzyme activities in the sedimentable and nonsedimentable fractions during calcium paradox. The lysosomal enzyme activities were also detected in the perfusate collected during reperfusion with calcium-containing medium. These changes occurred during the reperfusion period since no alterations were apparent after calcium-free perfusion and were dependent upon the time of reperfusion with medium containing Ca2+ as well as the time of perfusion with Ca2+ -free medium before inducing Ca2+ paradox. These data indicate that alterations in lysosomal enzymes owing to reinstitution of calcium in Ca2+-deprived hearts may occur as a part of cardiac damage and general cellular disintegration.

摘要

尽管用无钙培养基短暂灌注心脏,随后用含钙培养基再灌注会导致明显的结构紊乱(钙反常),但这种细胞损伤的机制仍远未明确。由于溶酶体酶的激活与病理损伤有关,本研究的目的是检测经历钙反常的大鼠心脏中几种溶酶体酶活性的变化。在经历钙反常的心脏匀浆中,β-乙酰氨基葡萄糖苷酶、β-半乳糖苷酶、α-甘露糖苷酶或酸性磷酸酶的活性未见明显变化。然而,在钙反常期间,可沉淀和不可沉淀部分的溶酶体酶活性发生了显著改变。在用含钙培养基再灌注期间收集的灌注液中也检测到了溶酶体酶活性。这些变化发生在再灌注期间,因为在无钙灌注后没有明显改变,并且取决于用含Ca2+的培养基再灌注的时间以及在诱导Ca2+反常之前用无Ca2+培养基灌注的时间。这些数据表明,在缺钙心脏中由于钙的重新引入导致的溶酶体酶变化可能是心脏损伤和一般细胞解体的一部分。

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