Genetic stability: the key to longevity?

被引:16
作者
Davidovic, M [1 ]
机构
[1] Clin Inst Geriatr Med, YU-11050 Belgrade, Yugoslavia
关键词
D O I
10.1054/mehy.1998.0767
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
In gerontology, there are abundant data indicating that functional cell capacity decreases with age. Clinical practice and the results of several studies have demonstrated that a high (depending on the study) percentage of people over eighty are practically 'normal' (successful aging). The hypothesis is that they are in fact in much the same position as the normal population of middle age. The reason for this may be the genetic stability of these persons. With time, the amount of damage to DNA rises and accumulates, which leads to cancer, heart problems and getting old. In genetically stable individuals, that period of accumulation is longer so they live longer. In humans, there appear to be two subgroups that age at different rates. The slower-aging group have better DNA repair systems. Genome stability plays a fundamental role in such age-related differences. The evolution of the human race would have been much slower if it had involved only genetically stable individuals. From the individual's point of view, however, it is better to have genetic stability. Regardless of the classical theory of aging, the lifespan of a species is related to metabolic rate. The apes and the humans have practically the same rate of metabolism, but humans live twice as long as apes. A similar phenomenon has been observed in other species and other tissues. Modification of DNA repair capacity plays a fundamental role in determination of the life span of a species. Genetic instability could be one of the basic reasons for senescence. The rise of chromosomal aberrations in long-lived persons is attributable to their genetic stability. They are practically in the same position as a normal population at middle age. Genetic instability is often associated with cancer and many different disorders of the immune system, which are frequent in the elderly. (C) 1999 Harcourt Publishers Ltd.
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页码:329 / 332
页数:4
相关论文
共 40 条
[1]   CYP2D6, NAT2 and CYP2E1 genetic polymorphisms in nonagenarians [J].
Agundez, JAG ;
Rodriguez, I ;
Olivera, M ;
Ladero, JM ;
Garcia, MA ;
Ribera, JM ;
Benitez, J .
AGE AND AGEING, 1997, 26 (02) :147-151
[2]   STUDIES ON DNA-REPAIR DEFECTS IN DEGENERATIVE BRAIN DISEASE [J].
BOERRIGTER, METI ;
VIJG, J .
AGE AND AGEING, 1993, 22 (01) :S44-S52
[3]  
BULPITT CJ, 1994, J HUM HYPERTENS, V8, P631
[4]  
CAPURSO A, 1944, IAG CLIN SECT C FLOR, P102
[5]  
CRAWFORD J, 1984, ANN REV GERONTOLOGY, P3
[6]  
DAVIDOVIC M, 1995, AGE VAULT, P235
[7]   INCREASED CHROMOSOMAL INSTABILITY IN LYMPHOCYTES FROM ELDERLY HUMANS [J].
DUTKOWSKI, RT ;
LESH, R ;
STAIANOCOICO, L ;
THALER, H ;
DARLINGTON, GJ ;
WEKSLER, ME .
MUTATION RESEARCH, 1985, 149 (03) :505-512
[8]   CHROMOSOMES OF OLDER HUMANS ARE MORE PRONE TO AMINOPTERINE-INDUCED BREAKAGE [J].
ESPOSITO, D ;
FASSINA, G ;
SZABO, P ;
DEANGELIS, P ;
RODGERS, L ;
WEKSLER, M ;
SINISCALCO, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (04) :1302-1306
[10]  
HALLGREN HM, 1985, J MED TECHNOL, V2, P685