Induction of apoptosis in rat myocardium under anoxic conditions

被引:9
作者
Saprunova, VB [1 ]
Kazimirchuk, SA [1 ]
Tonshin, AA [1 ]
Bakeeva, LE [1 ]
Yagujinsky, LS [1 ]
机构
[1] Moscow MV Lomonosov State Univ, Belozersky Inst Physicochem Biol, Moscow 119899, Russia
关键词
apoptosis; anoxia; cardiomyocytes; myocardial infarction; mitochondria; electron microscopy;
D O I
10.1023/A:1014426400741
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The effect of anoxic incubation of small slices of isolated rat hearts on respiration, internucleosomal DNA fragmentation, and mitochondrial ultrastructure was investigated. Anoxic incubation for 72 h induced apoptosis accompanied by internucleosomal DNA fragmentation and changes in respiration and mitochondrial ultrastructure. The mitochondrial population was characterized by morphological heterogeneity. In a significant part of the mitochondrial population there were signs of mitochondrial swelling and appearance of electron-dense mitochondria. Anoxia also induced the appearance of an atypical (and previously unknown) population of small electron-dense mitochondria. They were characterized by unusual localization inside electron-light mitochondria. Under anoxic conditions the inner mitochondrial membrane formed electron-dense ordered structures. All changes described here reflect two opposing processes occurring in mitochondria: apoptotic destruction and compensatory processes responsible for maintenance of mitochondria.
引用
收藏
页码:246 / 253
页数:8
相关论文
共 20 条
[1]   ENDOTOXIN-INDUCED SERUM FACTOR THAT CAUSES NECROSIS OF TUMORS [J].
CARSWELL, EA ;
OLD, LJ ;
KASSEL, RL ;
GREEN, S ;
FIORE, N ;
WILLIAMSON, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1975, 72 (09) :3666-3670
[2]   Unresolved issues regarding the role of apoptosis in the pathogenesis of ischemic injury and heart failure [J].
Elsässer, A ;
Suzuki, K ;
Schaper, J .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2000, 32 (05) :711-724
[3]   CONFORMATIONAL BASIS OF ENERGY TRANSFORMATIONS IN MEMBRANE SYSTEMS .3. CONFIGURATIONAL CHANGES IN MITOCHONDRIAL INNER MEMBRANE INDUCED BY CHANGES IN FUNCTIONAL STATES [J].
GREEN, DE ;
ASAI, J ;
HARRIS, RA ;
PENNISTON, JT .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1968, 125 (02) :684-+
[4]  
JAMES TN, 1993, J LAB CLIN MED, V122, P309
[5]   NORMAL AND ABNORMAL CONSEQUENCES OF APOPTOSIS IN THE HUMAN HEART - FROM POSTNATAL MORPHOGENESIS TO PAROXYSMAL ARRHYTHMIAS [J].
JAMES, TN .
CIRCULATION, 1994, 90 (01) :556-573
[6]   APOPTOSIS - BASIC BIOLOGICAL PHENOMENON WITH WIDE-RANGING IMPLICATIONS IN TISSUE KINETICS [J].
KERR, JFR ;
WYLLIE, AH ;
CURRIE, AR .
BRITISH JOURNAL OF CANCER, 1972, 26 (04) :239-+
[7]   The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol [J].
Kluck, RM ;
Esposti, MD ;
Perkins, G ;
Renken, C ;
Kuwana, T ;
Bossy-Wetzel, E ;
Goldberg, M ;
Allen, T ;
Barber, MJ ;
Green, DR ;
Newmeyer, DD .
JOURNAL OF CELL BIOLOGY, 1999, 147 (04) :809-822
[8]  
KROLENKO SA, 1979, TSITOLOGIYA+, V21, P1016
[9]   Increased apoptosis in the heart of genetic hypertension, associated with increased fibroblasts [J].
Liu, JJ ;
Peng, LM ;
Bradley, CJ ;
Zulli, A ;
Shen, J ;
Buxton, BF .
CARDIOVASCULAR RESEARCH, 2000, 45 (03) :729-735
[10]   Mitochondria-dependent apoptosis and cellular pH regulation [J].
Matsuyama, S ;
Reed, JC .
CELL DEATH AND DIFFERENTIATION, 2000, 7 (12) :1155-1165