MYOCARDIAL AGING - ANTIOXIDANT ENZYME-SYSTEMS AND RELATED BIOCHEMICAL-PROPERTIES

被引:75
作者
JI, LL [1 ]
DILLON, D [1 ]
WU, E [1 ]
机构
[1] UNIV ILLINOIS, DIV NUTR SCI, URBANA, IL 61801 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1991年 / 261卷 / 02期
关键词
MYOCARDIUM; LIPID PEROXIDATION; EXERCISE;
D O I
10.1152/ajpregu.1991.261.2.R386
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The effects of aging on myocardial antioxidant enzyme activity, lipid peroxidation, and other related biochemical properties were investigated in male Wistar-Furth rats at 4,26, and 31 mo of age at rest and after an acute exercise bout. The results showed that resting heart cytosolic superoxide dismutase (CuZn SOD) activity was significantly decreased in the heart with aging (66 +/- 6.5 U/mg protein at 4 mo vs. 49 +/- 3.8 U/mg protein at 31 mo) and was elevated in all age groups after exercise. Mitochondrial Mn SOD activity was almost doubled in both 26- and 31-mo-old rats compared with that at 4 mo. Myocardial catalase and cytosolic glutathione peroxidase (GPX) activities were significantly decreased with age, whereas mitochondrial GPX was 29% higher (P < 0.05) in 31- than 4-mo-old rats. Glutathione S-transferase activity in the heart also declined with age (P < 0.05 at 31 mo). Malondialdehyde contents in both heart homogenate and mitochondria were significantly increased at old age. Activity of several enzymes related to myocardial energy production, e.g., citrate synthase, malate dehydrogenase, and lactate dehydrogenase, as well as myocardial protein content showed an age-related decline. These data indicate that myocardial antioxidant capacity is weakened during aging and that the compensatory increases of mitochondrial SOD and GPX may be an important mechanism in coping with free radical damage in senescent heart. Findings in the present investigation seem to support the free radical theory of aging.
引用
收藏
页码:R386 / R392
页数:7
相关论文
共 30 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   HYDROPEROXIDE METABOLISM IN MAMMALIAN ORGANS [J].
CHANCE, B ;
SIES, H ;
BOVERIS, A .
PHYSIOLOGICAL REVIEWS, 1979, 59 (03) :527-605
[3]  
DAS DK, 1987, BIOL NEONATE, V51, P156, DOI 10.1159/000242647
[4]   FREE-RADICALS AND TISSUE-DAMAGE PRODUCED BY EXERCISE [J].
DAVIES, KJA ;
QUINTANILHA, AT ;
BROOKS, GA ;
PACKER, L .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1982, 107 (04) :1198-1205
[5]   MULTIPLE RANGE AND MULTIPLE F TESTS [J].
DUNCAN, DB .
BIOMETRICS, 1955, 11 (01) :1-42
[6]  
FLOHE L, 1984, METHOD ENZYMOL, V105, P114
[7]   ROLE OF OXYGEN RADICALS IN CARDIAC INJURY DUE TO REOXYGENATION [J].
GAUDUEL, Y ;
DUVELLEROY, MA .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1984, 16 (05) :459-470
[8]  
HABIG WH, 1974, J BIOL CHEM, V249, P7130
[9]   BIOENERGETICS IN AGING [J].
HANSFORD, RG .
BIOCHIMICA ET BIOPHYSICA ACTA, 1983, 726 (01) :41-80
[10]   AGING - A THEORY BASED ON FREE-RADICAL AND RADIATION-CHEMISTRY [J].
HARMAN, D .
JOURNALS OF GERONTOLOGY, 1956, 11 (03) :298-300