Child: Environmental and genetic factors affect the aging process. Gene control plays a key role. Aging is not determined by a single gene, but the result of a series of activation and retardation of "aging gene" and "longevity gene" and the interaction of their products. DNA (especially mitochondrial DNA) is not as stable as originally thought. The genetic control system, including genes, will be affected by the internal and external environment, especially the damage factors such as oxygen free radicals, which will accelerate the aging process. In the case of imperfect environment, the environment is an important factor affecting aging. For example, before liberation, the average life expectancy in China was only 35 years old, and now the average life expectancy of Beijing residents is about 76 years old. China also has longevity places, such as Hotan in Xinjiang, Nantong in Jiangsu and Bama in Guangxi, which shows that the environment is very important. What ordinary people can do to delay aging is to improve the environment as much as possible. However, in the same longevity village, why don't everyone live long? This also shows that heredity plays a key role. In common areas, there are often longevity families, indicating that longevity genes can be expressed through heredity.

The World Health Organization defines 60 as the beginning of old age. People's aging, like spring, summer, autumn and winter, and bloom flowers falling, are all beautiful phenomena in nature. Although people can't live forever, we can pursue health and longevity. Exploring the mystery of longevity is an arduous mission of the medical community. What should I do if I am not old before 80, 90 or even 100, or if I am sick and painless? Therefore, the author specially visited China Academy of Sciences, the director of Peking University Aging Research Center and Professor Tong of Peking University Health Science Center, who initially solved the mystery of aging in China.

The natural life span of human beings is about 120 years.

What is the life reference of Beijingers?

Tong Tanjun: Buffon, a famous French biologist, pointed out that the life span of mammals is about 5-7 times that of the growing period, which is usually called Buffon's life coefficient. The growth period of human beings is about 20-25 years, and the estimated natural life span of human beings is 100- 175. Hayfrick proved that human fibroblasts can undergo about 50 mitoses from embryo to adult to death, each cell cycle is about 2.4 years, and the natural life span of human beings should be about 120 years. Although different scholars have different answers, the conclusions are basically the same. At present, it is generally believed that the natural life span of people is about 120 years old.

Beijing Reference: 100 Will the life span of future generations be 120 years?

Tong: The average life span is greatly influenced by the environment, but the maximum life span of various animals is quite stable. The maximum life span of rodents is about 3 years, monkeys are about 28 years, dogs are about 34 years, elephants are about 62 years, and humans are about 120 years old. After 100 years, the maximum life span of mice is still 3 years. But after 100 years, the average life expectancy of people will inevitably increase. For example, before and after the liberation of our country, the average life expectancy increased greatly. It is difficult to improve the maximum life span of human beings, and genetic modification must be carried out. Although scientists have successfully experimented on fruit flies and worms, introducing some genes or mutating some genes in them can prolong their maximum life.

Beijing Reference: As an individual, can people's life expectancy be predicted?

Tong Tanjun: How long is the life expectancy? Is what many people want to know. In order to cater to this psychology, some informal medical books at home and abroad have published life prediction methods. The main basis of prediction is to list some factors that affect health. Those that are beneficial to health will be increased by one to several years according to the nature or degree, and those that are unfavorable to health will be reduced by one to several years according to the nature or degree. Finally, add all the data to get the sum, and then add and subtract with a fixed life index or life base to get the predicted life. But in real life, how do genes control aging evolution at different stages of human development? I still don't know. Therefore, there is no recognized method to correctly predict human life span in the world at present.

The lungs are the most prone to aging.

Beijing Reference: When do people get old? Is there an aging order for human organs?

Child: Aging is divided into physiological aging, physiological aging and pathological aging. Different individuals of the same species, even different tissues or organs of the same individual, have different aging rates. From birth to 16 years old, the functions of various tissues and organs increase rapidly, and the period from 16-20 years old to 30-35 years old is stationary. From the age of 35, the function of some organs and tissues began to decline, and the aging rate accelerated with age. If the function of tissues and organs of a 30-year-old person is 100, the functions will decrease as follows: (at rest) the nerve conduction velocity will decrease by 0.4%, the cardiac output will decrease by 0.8%, the renal filtration rate will decrease by 1.0%, and the maximum respiratory volume will decrease by1. It can be understood that the lungs are the most prone to aging. Followed by the glomerulus of the kidney, then the heart, while the aging speed of nerve and brain tissue is relatively slow. With the increase of age, the function of tissues and organs decreases linearly, which is a universal law, so the elderly are prone to get sick. But in real life, some people's aging speed and biological indicators of aging.

Beijing Reference: So, what does it mean that people are getting old?

Tong: An important factor that restricts the study of mammalian aging is the lack of reliable and easy-to-measure biological age evaluation markers. We have found some indicators at the cellular and molecular levels, which can be used as biomarkers of aging, but at present, they are only in the laboratory stage, and there is still a long way to go before they are applied to life. The following five indicators are all related to aging, but they all have shortcomings when used alone:

1. Proliferation ability of fibroblasts in vitro. According to the hypothesis of cell aging, the proliferation ability of fibroblasts in vitro is a reliable index to estimate the aging degree of donors.

Second, the ability to repair DNA damage. Many kinds of DNA damage, such as chromosome translocation, DNA single and double strand breaks, fragment deletion and so on, accumulate with age. This phenomenon is not only related to the increase of free radical production rate and the decrease of antioxidant level during aging, but also closely related to the decrease of DNA repair ability. The indexes for evaluating DNA repair ability include unscheduled DNA synthesis, DNA polymerase B and endonucleases deoxyribonuclease UV2DNase and AP2DNase. In addition, the methods of detecting various DNA damage can also be used to detect the repair ability of such DNA damage.

Third, mitochondrial DNA fragments are missing. The detection of mitochondrial DNA fragment deletion can be based on hair, which is very convenient to use and is a good biomarker of aging.

Fourth, the level of DNA methylation. DNA methylation is an important mechanism for the gradual regulation of gene expression in eukaryotes. By changing the chromosome structure, the interaction between DNA and protein is affected, and the gene expression is inhibited.

Fifth, the length of telomeres. Telomere length in different tissues of human body was detected, and it was found that telomere length was related to cell life. Sperm and embryo have the longest telomeres, while small intestinal mucosal cells have the shortest telomeres. Zglinicki et al reported that single strand breaks caused by oxidative stress are the main reason for telomere shortening. Hydrogen peroxide induces cell senescence phenotype and accelerates telomere shortening. Therefore, telomere length is not only a "counter" of cell division times, but also a sign of cell aging.

Improve the environment and change the aging.

Beijing Reference: What are the factors closely related to aging?

Child: Environmental and genetic factors affect the aging process. Gene control plays a key role. Aging is not determined by a single gene, but the result of a series of activation and retardation of "aging gene" and "longevity gene" and the interaction of their products. DNA (especially mitochondrial DNA) is not as stable as originally thought. The genetic control system, including genes, will be affected by the internal and external environment, especially the damage factors such as oxygen free radicals, which will accelerate the aging process. In the case of imperfect environment, the environment is an important factor affecting aging. For example, before liberation, the average life expectancy in China was only 35 years old, and now the average life expectancy of Beijing residents is about 76 years old. China also has longevity places, such as Hotan in Xinjiang, Nantong in Jiangsu and Bama in Guangxi, which shows that the environment is very important. What ordinary people can do to delay aging is to improve the environment as much as possible. However, in the same longevity village, why don't everyone live long? This also shows that heredity plays a key role. In common areas, there are often longevity families, indicating that longevity genes can be expressed through heredity.

The length of terminal zone decreases with age, and women live longer than men.

Beijing Reference: Is there a gender difference in human aging?

Tong: Epidemiological investigation shows that human women live longer than men. How to explain the universal life phenomenon that women live longer than men from the molecular level? This has to start from the aging mechanism, such as oxygen free radical theory, modern DNA damage repair theory, mitochondrial damage theory, terminal region hypothesis and so on. In the following, we will combine our own research work to introduce the hot spots of aging research in the world as follows: except stem cells, the length of most human somatic cells decreases with age, while the length of cells cultured in vitro decreases with passage times; When the terminal region is shortened to a certain extent, cells will no longer divide, that is, they will not be passed on to generations, and eventually they will age and die. Terminal region refers to the special structure at the ends of chromosomes, which can prevent the cross-linking of DNA chains at the ends of two chromosomes (also called deoxyribonucleic acid, which is genetic material containing genetic information) and lead to chromosome aberration. It is found that the length of male terminal area is longer than that of female in the same age group, but it shortens faster than that of female with age, with a difference of 3bp every year.

Beijing Reference: Can People Change Aging?

Tong: Sports medicine experts show that cardiopulmonary function, osteoporosis, muscle strength, physical endurance, cholesterol level and blood pressure can all be improved through long-term exercise or physical labor and health care. It is difficult to improve the index, only the hair turns white, the skin elasticity decreases, and it shrinks and thins. From the molecular level, we found that the tumor suppressor gene p 16 can affect telomere length by regulating the activity of 1Kb protein, but not by telomerase.

DNA repair ability and cell life, it is preliminarily clear that p 16 is the main link in the genetic control program of human cell aging. This is a breakthrough in the study of human cell aging mechanism in China, and it is also found that the aging-related gene p2 1 can protect aging cells from apoptosis. As for which genes control aging and how to control the speed of aging, it is a subject that human beings will continue to study.

Beijing Reference: How do ordinary people delay aging at present?

Child: Improve the internal and external environment-follow the principles of balanced diet, moderate exercise and psychological balance. For good environmental factors, we make full use of them; For the bad factors, we should understand it and standardize it. Ordinary ordinary relaxed Beijing reference: Tong Lao, how old are you this year? You look very energetic. Please tell us your regimen.

Tong: I am 7 1 year old. Old people should live a normal life without stress.

I think the most important thing for the health of the elderly is to be flexible in legs, hands and feet, instead of always sitting still or lying down. If you are competent for long-distance walking, it reflects good heart function. It is worth mentioning that the elderly don't watch TV for several hours. Be ordinary about your diet, don't be too picky, and don't avoid eating. For example, I will take a bite of fat, but the total amount should not be too much. Psychologically, we should do something happy to relax ourselves. For example, when climbing a mountain, you can think nothing. The life of the elderly after retirement can also be wonderful, but don't be too tired; Helping to take care of grandchildren is actually the happiest thing.

Proud of advocating science and ashamed of ignorance.

Beijing Reference: What did you think when you were engaged in aging research?

Tong: According to statistics, two-thirds of a person's lifetime medical expenses are spent in old age. With the increase of the elderly, their medical expenses will become a heavy burden on families and society, so gerontology is becoming more and more important. The purpose of aging research is to improve the quality of life of the elderly, prolong the healthy period and shorten the sick period, not just live for a few more years. Aging research is a young subject. In the past, the research direction was the whole organ research, now it is at the cellular level, and model animal research will be done in the future, but the direct results of animal research can not be applied to people. Therefore, the study of aging should be diversified, not only at the cellular level, but also at the organ level and the overall level, so that the study of aging mechanism can keep up with the international and times. The basic research of geriatrics plays an important role in geriatric clinical medicine. The basic research of gerontology in China is still relatively weak, so it is difficult to catch up with the backwardness. We should be proud of advocating science and ashamed of ignorance. Although China is a country with a large population, the research on aging is not contradictory and should be among the advanced countries in the world.

American scientists' new understanding of aging: human life span can be changed.

February 7, 2005 09: 12 Xinhuanet

In the issue of 65438+ 10/7, Newsweek published an article entitled "Wrinkles of Years", which introduced five scientists' new explanations on the biochemical process of aging. They have a consensus that human life span is not fixed. The article is summarized as follows:

Although death is as inevitable as paying taxes, in the future, people's aging process will slow down and their life span will be significantly prolonged. Five scientists put forward a new explanation for the biochemical process of aging, which opened the door for the emergence of drugs to prolong life. Although their research methods are different, they all have a common understanding that human life span is not fixed. Enhancement: The target gene is more active in anti-aging. A few years ago, students of molecular geneticist Cynthia kenyon took a plate of earthworms and asked passers-by how big they thought these earthworms were. Most people say it's only five days. They didn't know that kenyon had repaired the genes of these earthworms. The health of these squirming creatures looks exactly the same as they did five days ago, but in fact they have been born 144 days-six times the normal life span.

In the past ten years, kenyon's persistent research shows that by changing hormone levels and enhancing the functions of about 65,438+000 genes, "life span can be easily changed greatly", at least for earthworms. Some of these genes can produce antioxidants; Some can make natural fungicides; Others participate in transporting fat to the whole body; Others are called guardians. According to kenyon, they "can keep cell components in good working condition". Generally speaking, the more active these genes are, the longer the life span of organisms may be.

1993, the research results of earthworm genes in kenyon were published for the first time. Skeptics predict that this result will not work in humans. Scientists still don't know the exact reason why the life span of human beings and earthworms is so different, let alone what changing the life span of earthworms may mean to human beings. But the cell composition of earthworms is very similar to that of higher mammals. This discovery opened the door for Changsheng Company, which produces healthy and nutritious products. The company is trying to develop a drug that can produce the same effect as genetic modification in kenyon. Kenyon said: "I am not saying that by changing some genes, human beings can live forever, but can make an 80-year-old man look like 40 years old." Who would object to this?

Stress: Long-term stress will make cells age faster.

If you complain that stress adds new wrinkles or gray hair, you may be right.

A research report published in the Proceedings of the National Academy of Sciences last fall provided a scientific basis for your point of view. Eliza Epel, an assistant professor of psychiatry at the University of California who participated in the study, and her colleagues found that being nervous for a long time, or just feeling nervous, can significantly shorten the length of telomeres. Telomeres are centromeres at the end of chromosomes in cells, which can be used to measure the aging process of cells. The shorter telomeres are, the shorter the life span of cells will be, and the faster the human body will age.

Epel studied 39 women between the ages of 20 and 50. Some of their children suffer from serious chronic diseases, such as cerebral palsy. Epel compared them with another 65,438+09 healthy mothers in the same age group. The longer a mother takes care of a sick child, the shorter her telomeres will be, and the greater the oxidative stress (the process of releasing free radicals that damage DNA) she will face. Compared with the women who feel the least stress, the telomeres of the women who claim to be the most stressed in the two groups are equivalent to those who are 10 years older than them.

Although Epel admits that more research is needed to confirm her findings, she thinks this result may be positive. She said: "Since we think we can see that stress can cause intracellular damage, people may pay more attention to mental health." She added that there is "absolute" hope to reverse DNA damage. "Changing lifestyle and learning to reduce stress may improve the quality of life, improve mood and prolong life."

Restriction: Strict control of calorie intake may slow down the aging rate.

1986, when Leonard Guarente first proposed to study biological aging by limiting calorie intake, the idea sounded ridiculous. However, in the past ten years, researchers have mainly understood why the sudden reduction of calorie intake can stimulate the activity of a gene called SIR2 and prolong the life span of simple organisms, and made great progress.

Guarente and David Sinclair, a researcher from Harvard University, are top experts in this field. They mainly study the anti-aging enzyme named "sirtuins", which is a protein family produced by SIRT 1, similar to SIR2 or SIR2 in mammals. Guarente's experiments have clarified many basic molecular processes behind SIR2. For example, a natural chemical called NADH can inhibit the function of sirtuins; They have confirmed that yeasts with lower NADH content live longer. Sinclair found that resveratrol was related to calorie restriction. Studies have shown that the life span of yeast can be prolonged by 70% under the action of large dose of resveratrol.

Since few people are willing to significantly limit their calorie intake, Guarente began to look for a drug with the same effect. Changsheng Company has also begun to make use of Guarente's research results, which means that one day people may still benefit from calorie restriction without mentioning the word dieting.

Supplement: Two chemicals make mice young.

According to the research report published in the Proceedings of the National Academy of Sciences in 2002, Bruce Ames, a child medicine expert at Oakland Institute in California, and his colleagues gave mice two chemicals found in somatic cells-acetyl L-carnitine and α -lipoic acid. This not only makes the mouse perform better in solving problems and memory tests, but also makes it easier and more energetic to act.

Researchers have confirmed that mixing different chemicals can improve the function of mitochondria and organelles, which are the main energy sources of cells. In one study, Ames found that lipoic acid can protect cells from oxidation when iron peroxide or hydrogen peroxide is added.

Aging: Looking at Essence through Phenomena

I. Introduction

At present, the research on aging mechanism in life science is in a period of blooming and fruitful results (Comfort,1979; Medvedev,1990; Hayflick,1998; Kirkwood,1999; Warner, 2005; Yin & Chen, 2005) However, due to the extremely complicated aging process, ever-changing influencing factors, and the knowledge limitation and professional prejudice of researchers in various fields, we are actually faced with a mixed bag of fish and dragons (Medvedev,1990; Olshansky et al., 2002; De Grey et al., 2002; De Magalhaes, 2005).

This paper will first briefly review the important progress in the study of aging mechanism, and discuss the interaction between genetic regulation and inevitable environmental damage during aging. Then, we emphasize that in order to study the real aging process, we should pay attention to various physiological aging changes in a healthy state, not pathological changes. For example, aging-related protein degeneration is the most common aging phenomenon in organisms. After expounding the biochemical processes of free radical oxidation and non-enzymatic glycosylation and the biochemical mechanism of the formation of entropy-increasing senile pigment, the special significance of carbonyl poisoning (stress) in the aging process was emphatically discussed (Yin & Brunk， 1995)。 Finally, through the phenomenon to see the essence, it is pointed out that the biochemical side effect injury and disrepair accumulation are the biochemical essence of physiological aging process.

Second, an overview of aging theory and research on aging mechanism.

A large number of life phenomena and experimental facts show that although the death of a few lower animals shows that some mysterious "life switch" is working, the aging process, especially the aging process of higher animals in adulthood, has been clearly regarded as a slow and gradual process of injury and defense against environmental factors. At present, a large number of important research results on aging show this point indisputably (Comfort,1979; Medvedev,1990; Hayflick,1998; Yin, 2002). In order to facilitate analysis and discussion, let's first list dozens of the most important aging theories to date:

The whole aging theory mainly includes: wear aging theory (Sacher 1966), false aging theory (Orgel 1963), metabolic rate aging theory, self-poisoning aging theory (Metchnikoff 1904), natural evolution aging theory (program control theory) and residual information theory (program control theory)

Organ-level aging theories include: brain decline theory, ischemic injury theory, endocrine decline theory (Korencheysky, 196 1) and immune decline theory (Wolford1969); );

The aging theories at the cellular level are: cell membrane aging theory (Zs. -Nagy, 1978), somatic mutation aging theory (Szilard, 1959), mitochondrial damage aging theory (Miquel et al., 1980), lysosomal aging theory (lipofuscin).

The aging theories at molecular level include telomere shortening theory (programmed theory), gene modification theory, DNA repair defect theory (Vilenchik, 1970), free radical theory (Harman, 1956, 2003) and oxidative aging theory (Sohal & Allen， 1990； Yu & Yang, 1996), non-enzymatic glycosylation aging theory (Cerami, 1985), carbonyl poisoning aging theory (Yin&; Brunk, 1995) and trace element aging theory (Eichhorn, 1979) and so on.

Other important aging theories include entropy increasing aging theory (Sacher 1967, Bortz, 1986), mathematical aging theory and various comprehensive aging theories (Sohal,1990; Zs。 -Naji,1991; Kowald & Kirkwood, 1994). From the above 26 main theories of aging, it can be seen that the vast majority of aging theories (22 kinds) think that aging is the result of various external injuries in the process of life. In short, it is a passive injury accumulation process.

It should be noted that among the four aging theories classified as "programmed theory", the so-called "cell aging" observed and studied by cell division limit theory and telomere shortening theory is very different from the aging of animals as a whole. As far as the concept of "cell does not divide" is concerned, it is not synonymous with "cell aging". The explanation is simple. Terminal differentiated nerve cells and most muscle cells do not divide after differentiation in early life (fetus or baby), but remain healthy in animals for life (Sohal,1981; Berta, 1990). Recently, Lanza et al. used fetal bovine diploid fibroblasts close to the multiplication limit in vitro as donor cells, and even successfully cultivated six cloned cattle (Lanza et al., 2000). The telomeres of these six cloned cattle are longer than those of sexually propagated cattle of the same age. In fact, from the common sense of the aging process (or definition: aging is a process in which various functions of the body are generally weakened and the ability to resist environmental damage and restore internal balance is gradually reduced), telomere shortening has nothing to do with the decline of aging sexual function of cells and animals as a whole. Limited by space, this paper will not discuss it in detail (Wakayama et al. 2000Cristofalo et al., 2004).

The understanding of how genetic factors and environmental damage affect the aging process in life science has gone through a long stage of "mutual confirmation". After decades of hard exploration by gene life scientists, dozens of genes related to aging and longevity have been identified through experiments (finch &; Tanzi1997; Warner, 2005; ), such as: age-1, chico, CLK- 1, DAF-2, DAF- 16, DAF-23, EAT-2, GRO- 1, HSF-/kloc-0. ISP- 1，Klotho，LAG- 1，LAC- 1，MSRA，MTH，α MUPA，Old- 1，P66SH，Hamet & PIT- 1，Prop-65438。 Tremblay, 2003; Warner, 2005). These life-related genes can be roughly divided into four categories: 1) anti-stress genes (such as anti-thermal shock and anti-oxygen stress); 2) Genes related to energy metabolism (such as insulin/insulin factor signaling pathway, food restriction or mitochondrial related genes); 3) Anti-damage and mutant genes (such as protein and the repair and renewal of genetic factors); 4) Stabilize genes related to neuroendocrine and mammalian spermatogenesis. The biological functions of many "longevity genes" are still unclear.

In addition, CDK 1, MAPK, 1 and P 16 (Wang et al., 2001; De Magalhaes, 2005). Therefore, life scientists have clearly realized that there are genes related to aging and longevity, but the genetic factors that control the length of life are not one or several, nor one or several groups, but the result of the interaction of hundreds of genetic factors (Holliday, 2000; Warner, 2005). The aging process is related to physiology and pathology, and many gene networks in many regulation, defense, repair and metabolism systems cooperate to resist various environmental injuries. In a word, aging is the result of the interaction of congenital (genetic) factors and acquired (environmental) factors, which has gradually become a recognized scientific fact in the field of aging biology research.

Recognizing the above characteristics of animal aging, the study of aging mechanism can rationally focus on the scope of damage accumulation and defense repair (molecular level).

Third, the physiological characteristics of aging and potential molecular killers.

In order to explore the real aging mechanism, it is necessary to make a clear definition of aging and senile diseases. Generally speaking, the academic community generally agrees that aging is not a disease. The aging mechanism mainly studies the physiological aging changes in the healthy state of the body.

Considering that the aging process is a universal, gradual, cumulative and irreversible physiological process, the cause of physiological aging should be * * * injury factor (Strehler, 1977). The cumulative and irreversible changes caused by these factors are the aging changes that represent the practical significance.

In fact, aging changes at the whole level, organ level or cell level are ultimately changes at the molecular level, and they are just different manifestations of changes at the molecular level at different levels. Many non-disease aging changes, such as the increase of blood pressure caused by aging arteriosclerosis, the decrease of lung fiber elasticity and vital capacity caused by collagen cross-linking, as well as skin relaxation, vision loss and joint stiffness, all imply the internal changes of biomacromolecules (Bailey, 200 1). These changes are not sick from the perspective of the whole and tissues and organs, but the molecular structure has been "sick". For example, protein's cross-linking hardening is one of the most common biochemical "shackles" that constantly stifle vitality. Even the old man who died of illness, the basic structure of protein in his body has long been unrecognizable compared with that of young people. Protein degeneration and modification related to aging in organisms is a common aging phenomenon. The aging body can observe the aging protein damage from the inside out and from top to bottom.

Of course, many scholars will not hesitate to agree that genetic damage should be one of the important causes of aging. However, the hypothesis that the aging process is somatic mutation accumulation has been ruthlessly refuted by rigorous scientific experiments. For example, the mutation of genetic factors caused by radiation damage should lead to obvious differences in life span between haploid wasps and diploid wasps, but the research results show that there is no obvious difference in life span between diploid wasps and haploid wasps whose DNA structure is damaged by double radiation, which denies the above speculation (Clark & Rubin,1961; Lamb, 1965). In addition, a large number of biomedical studies show that the increase of DNA damage and mutation during aging mainly leads to pathological changes (Bohr, 2002; Warner, 2005), for example, diseases that cause various mitochondrial DNA (Holliday, 2000; Wallace, 2003) and carcinogenesis. Considering that the aging process has obvious physiological characteristics, protein's age-related injuries and changes have obviously made more "practical contributions" to "real aging" than genetic materials (Kirkwood,1999; Riazanov Company; Nevsky, 2002; Yin & Chen, 2005).

In addition, Orgel (1963) put forward the "theory that mistakes lead to aging", which holds that aging is the gradual degradation of organisms' correct maintenance of protein synthesis, and it is basically denied because of the strong challenge of scientific experiments (Gallant & palm er 1979； Harley CB et al., 1980). The research of Harley et al. (1980) shows:' During the aging process of human fibroblasts cultured in vitro, the synthetic error of protein has not increased' (note that for protein, oxidative stress is almost an omnipresent and ever-present life killer). In addition, scientists in this field are increasingly aware that protein's post-expression degeneration is the most important manifestation of life activities and aging. Because protein allosteric changes related to aging can be seen everywhere in all parts of the aging body (such as aging fibrosis of various organs and tissues and accelerated fibrosis of various diseases), protein's aging injury in tissues is the last and most common aging phenomenon. In fact, almost every aging hypothesis involves aging protein damage. Therefore, the analysis and discussion of this thesis will focus on the correlation between protein's injury and repair and aging.

Generally speaking, the synthesis, loss and renewal of protein run through the whole life process. After the maturity of life, the synthesis and degradation (speed) of protein are in a dynamic balance. With the increase of age, this balance gradually inclines (Bailey, 2001; Terman, 200 1). There are many reports about the damage and changes of structural proteins and functional proteins in aging biological cells (Stadtman, 1992, 2003; Rattan,1996; Riazanov Company; Nef