Coping in longitudinal perspective: Findings from the bonn longitudinal study on aging

Within the Bonn Longitudinal Study on Aging (BOLSA) 221 women and men, born between 1890–95 and between 1900–05, were tested and interviewed in the year 1965 for the first time. Survivors were followed at seven measurement points until 1980. One of three lengthy interviews was related to the topic of stress and coping. Information on perceived stresses in the areas of housing, income, family and health were rated. Furthermore, responses to these different stress areas were analyzed by an empirically developed classification system. Findings point to a complex system of response patterns even in the group of very old participants. These response patterns were different for the four areas of stress, such as family or health etc. Response patterns related to the same problem area remained consistent over the 15-year span. Cluster analyses point to situation specific as well as person specific response patterns.This paper was originally presented at the XIV International Congress of Gerontology, Acapulco, Mexico, 18–23 June 1989.     

The mitochondrial theory of aging: Insight from transgenic and knockout mouse models

A substantial body of evidence has accumulated over the past 35 years in support of a role for oxidative damage to the mitochondrial respiratory chain and mitochondrial DNA in the determination of mammalian lifespan. The goal of this review is to provide a concise summary of recent studies using transgenic and knockout mouse models with altered expression of mitochondrial antioxidant enzymes (MnSOD (Sod2Tg and Sod2^+/−), thioredoxin 2 (Trx2^+/−), mitochondrial targeted catalase (mCAT) and mutant mice models that have been genetically manipulated to increase mitochondrial deletions or mutations (Polγ^D257A/D257A mutant mice) to examine the role of mitochondrial oxidative stress in aging. The majority of studies using these strategies do not support a clear role for mitochondrial oxidative stress or a vicious cycle of oxidative damage in the determination of lifespan in mice and furthermore do not support the free radical theory of aging. However, several key questions remain to be addressed and clearly more studies are required to fully understand the role of mitochondria in age-related disease and aging.     

Antioxidant-rich food intakes and their association with blood total antioxidant status and vitamin C and E levels in community-dwelling seniors from the Quebec longitudinal study NuAge

A cross-sectional study was designed to investigate the association between current consumption of a series of 26 common antioxidant-rich foods (ARF) with serum total antioxidant status (TAS) and plasma vitamin C and E levels in community-dwelling older adults. A convenience sample of the first 94 non-smoking Caucasian men (54%) and women (46%) enrolled in the Quebec Longitudinal Study NuAge were selected. The “Functional Foods Consumption Frequency Questionnaire” (FFCFQ) was administered at recruitment (T1) to ascertain patterns of consumption of ARF over the lifetime. The total Oxygen Radical Antioxidant Capacity (ORAC) of 25 ARF reported by subjects was estimated using published values. Serum TAS was determined based on the Trolox equivalent antioxidant capacity (TEAC) assay while plasma vitamins C and E (α- and γ-tocopherol) levels were analyzed by HPLC. The numbers of ARF eaten daily at T1, estimated from the FFCFQ and calculated from the diet recalls, were significantly correlated (r = 0.51, P < 0.0001) and each measure was associated with total ORAC content (r = 0.34, P < 0.001 and r = 0.59, P < 0.0001 for FFCFQ and recalls, respectively). No significant association was found between TAS and the total ORAC value of ARF determined from the quantitative 24-h diet recalls. However, daily ARF consumption at T1 obtained from the FFCFQ was significantly and positively correlated with TAS (r = 0.26, P < 0.05) and circulating levels of vitamin C (r = 0.25, P < 0.02) and α-tocopherol (r = 0.22, p < 0.05) and negatively correlated with plasma γ-tocopherol (r = − 0.25, P < 0.025). These results highlight associations between ARF consumption and circulating levels of antioxidants in the elderly and suggest benefits from antioxidant-rich foods during aging.     

Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction

AIM To comprehensively evaluate mitochondrial(dys) function in preclinical models of nonalcoholic steatohepatitis(NASH).METHODS We utilized two readily available mouse models of nonalcoholic fatty liver disease(NAFLD) with or without progressive fibrosis: Lep~(ob)/Lep~(ob)(ob/ob) and FATZO mice on high trans-fat, high fructose and high cholesterol(AMLN) diet. Presence of NASH was assessed using immunohistochemical and pathological techniques, and gene expression profiling. Morphological features of mitochondria were assessed via transmission electron microscopy and immunofluorescence, and function was assessed by measuring oxidative capacity in primary hepatocytes, and respiratory control and proton leak in isolated mitochondria. Oxidative stress was measured by assessing activity and/or expression levels of Nrf1, Sod1, Sod2, catalase and 8-OHdG. RESULTS When challenged with AMLN diet for 12 wk, ob/ob and FATZO mice developed steatohepatitis in the presence of obesity and hyperinsulinemia. NASH development was associated with hepatic mitochondrial abnormalities, similar to those previously observed in humans, including mitochondrial accumulation and increased proton leak. AMLN diet also resulted in increased numbers of fragmented mitochondria in both strains of mice. Despite similar mitochondrial phenotypes, we found that ob/ob mice developed more advanced hepatic fibrosis. Activity of superoxide dismutase(SOD) was increased in ob/ob AMLN mice, whereas FATZO mice displayed increased catalase activity, irrespective of diet. Furthermore, 8-OHd G, a marker of oxidative DNA damage, was significantly increased in ob/ob AMLN mice compared to FATZO AMLN mice. Therefore, antioxidant capacity reflected as the ratio of catalase:SOD activity was similar between FATZO and C57 BL6 J control mice, but significantly perturbed in ob/ob mice. CONCLUSION Oxidative stress, and/or the capacity to compensate for increased oxidative stress, in the setting of mitochondrial dysfunction, is a key factor for development of hepatic injury and fibrosis in these mouse models.     

Effect of aging, caloric restriction, and uncoupling protein 3 (UCP3) on mitochondrial proton leak in mice

Mitochondrial proton leak may modulate reactive oxygen species (ROS) production and play a role in aging. The purpose of this study was to determine proton leak across the life span in skeletal mitochondria from calorie-restricted and UCP2/3 overexpressing mice. Proton leak in isolated mitochondria and markers of oxidative stress in whole tissue were measured in female C57BL/6J mice fed ad-libitum (WT-Control) or a 30% calorie-restricted (WT-CR) diet, and in mice overexpressing UCP2 and UCP3 (Positive-TG), their non-overexpressing littermates (Negative-TG) and UCP3 knockout mice (UCP3KO). Proton leak in WT-CR mice was lower than that of control mice at 8 and 26 months of age. The Positive-TG mice had greater proton leak than the Negative-TG and UCP3KO mice at 8 months of age, but this difference disappeared by 19 and 26 months. Lipid peroxidation was generally lower in WT-CR vs. WT-Control mice and UCP3KO mice had greater concentrations of T-BARS (thiobarbituric acid reactive substances, a measure of lipid peroxidation) than did Positive-TG and Negative-TG. The results of this study indicate that sustained increases in muscle mitochondrial proton leak are not responsible for alterations in life span with calorie restriction or UCP3 overexpression in mice. However, UCP3 may contribute to the actions of CR through mechanisms distinct from increasing basal proton leak.     

Oxidative stress in testis of animals during aging with and without reproductive activity

The free radical theory of aging postulates that an imbalance between reactive oxygen species (ROS) and reactive nitrogen species (RNS) and antioxidant defenses is important in senescence. To address this issue and gain insight into the aging process, we have evaluated the antioxidant defenses and have assessed oxidative damage in testis tissues in aging male rats. In order to relate aging and reproduction, animals with and without reproductive activity were studied. In reproductive animals the results showed a progressive increase in antioxidant enzyme activity until 12 months of age followed by an abrupt fall at 24 months. In non-reproductive animals, antioxidant activity was stable through 12 months of age, but again, fell abruptly at 24 months of age. In addition, increased aconitase activity and increased testosterone levels were found among reproductively active animals. The data demonstrate the existence of metabolic differences in testis of reproductively experienced animals and reproductively naïve animals.     

Cytogenetic methods for detection of oxidative stress and evaluation of antioxidant therapy in hepatitis C infection

The plasma of patients with hepatitis C contains chromosome-damaging substances, the so-called "clastogenic factors" (CFs), as this is the case for other chronic inflammatory diseases and after radiation exposure. These endogenous clastogens, formed as a consequence of increased superoxide production by inflammatory cells, can be detected with cytogenetic methods, as they are used for exogenous clastogens. The long-lived, autosustained DNA-damaging effects of CFs are risk factors for the development of cancer and leukemia. In hepatitis C, the highest clastogenic scores has been observed in patients with hepatocellular carcinoma. In agreement with the link to inflammation, clastogenic score are correlated with necro-inflammatory scores in liver biopsies. Antioxidant therapy with a powerful superoxide scavenger resulted in normalization of clastogenic scores and significant decreases in aminotransferase levels, but did not influence the virus load. Preliminary results of our study on a limited number of patients suggest that pre-treatment with antioxidants may improve the outcome of interferon/ribavirin treatment. A comparison of a three-month treatment with either interferon alone or the antioxidant alone, yielded similar results for reduction of ALT levels, but only complete normalization of clastogenic scores for the antioxidant. Further studies have to be conducted to see whether a combination of an antiviral agent with an appropriate antioxidant would allow to reduce interferon and its side effects.Combination of antioxidants with IFN/RIBA was also reported by other authors with discordant results. The CF-test can be useful in clinical trials for the choice of the appropriate antioxidant.     

Mitochondria, reactive oxygen species, and chronological aging: a message from yeast

As a major intracellular source of reactive oxygen species (ROS), mitochondria are involved in aging and lifespan regulation. Using the yeast chronological aging model, researchers have identified conserved signaling pathways that affect lifespan by modulating mitochondrial functions. Caloric restriction and a genetic mimetic with reduced target of rapamycin signaling globally upregulate the mitochondrial proteome and respiratory functions. Recent discoveries support the notion that an altered mitochondrial proteome induces mitohormesis. Mitohormesis involves a variety of ROS during several growth stages and extends lifespan in yeast and other organisms. Here we recap recent advances in understanding of ROS as signals that decelerate chronological aging in yeast. We also discuss parallels between yeast and worm hypoxic signaling. In sum, this mini-review covers mitochondrial regulation by nutrient-sensing pathways and the complex underlying interactions of ROS, metabolic pathways, and chronological aging.     

Molecular basis for age-related changes in ileum: Involvement of Bax/caspase-dependent mitochondrial apoptotic signaling

Previous studies indicate that in the elderly, a morphological change in the small intestine is accompanied by apoptosis. However, currently little information is available on the molecular events leading up to the apoptotic process in aged ileum. Our current study assessed mitochondrial apoptotic signaling along with key factors known to be involved in mitochondrial permeabilization in rat ileum. Experimentations were carried out utilizing Sprague–Dawley rats at 6 and 24 months of age. The histological analysis showed a significant loss in thickness of the intestinal mucosa during aging, which was accompanied by higher reactive species. Molecular analysis revealed the mitochondrial translocation of Bax showed a significant increase with aging. However, the expression of cyclophilin D, adenine nucleotide translocator, and the voltage-dependent anion channel that regulates the mitochondria permeability transition pore decreased or remained unchanged. Furthermore, the expression of caspase 3 was enhanced in aged ileum with increased DNA fragmentation, while nuclear translocation of apoptosis-inducing factor and endonuclease G were decreased with aging.     

A 7-day profile of oxidative stress and antioxidant status in patients with acute liver failure

Purpose  Acute liver failure (ALF) is characterized by a rapid and massive destruction of hepatocytes. The role of oxidative stress in perpetuating the injury is undefined and may be a potential therapeutic target. Our aim was to study serial variation in oxidative stress and antioxidant status in patients with ALF. Methods  The study involved a prospective case–control study set in a tertiary care referral center. Thirty-two consecutive patients admitted with ALF were included with 23 healthy controls for comparison. Level of systemic oxidative stress as defined by superoxide dismutase (SOD), lipid peroxidation products (thiobarbituric acid reactive derivatives [TBARS]), and the total antioxidant capacity as the ferric reducing ability of plasma (FRAP) was measured at baseline on days 3 and 7. Results  The patients were aged 24 years (range 13–60 years) and included 20 females. Thirteen (40.6%) patients died. Patients with ALF had significantly increased systemic oxidative stress at presentation, as reflected by higher levels of SOD (P < 0.001) and TBARS (P < 0.001) than controls. Both TBARS levels and FRAP decreased progressively from admission to the end of first week among the survivors (P = 0.004 and 0.015, respectively). The antioxidant status reflected by FRAP (P = 0.001) was significantly lower in ALF patients than controls. No relation was found between the level of oxidative stress and the mortality or complications. Conclusion  A high level of systemic oxidative stress exists in ALF, with depletion of antioxidant reserves. Further studies are needed to define the clinical correlation of the large pro-oxidant burden.     

Influence of aerobic fitness on age-related lymphocyte DNA damage in humans: relationship with mitochondria respiratory chain and hydrogen peroxide production

The aim of this study was to analyze the influence of aerobic fitness (AF) on age-related lymphocyte DNA damage in humans, giving special attention to the role of the mitochondrial respiratory chain and hydrogen peroxide production. Considering age and AF (as assessed by VO₂max), 66 males (19–59 years old) were classified as high fitness (HF) or low fitness (LF) and distributed into one of the following groups: young adults (19–29 years old), adults (30–39 years old), and middle-aged adults (over 40 years old). Peripheral lymphocytes obtained at rest were used to assess DNA damage (strand breaks and formamidopyrimidine DNA glycosylase (FPG) sites through the comet assay), activity of mitochondrial complexes I and II (polarographically measured), and the hydrogen peroxide production rate (assayed by fluorescence). Results revealed a significant interaction between age groups and AF for DNA strand breaks (F = 8.415, p = .000), FPG sites (F = 11.766, p = .000), mitochondrial complex I activity (F = 7.555, p = .000), and H₂O₂ production (F = 7.500, p = .000). Except for mitochondrial complex II activity, the age variation of the remaining parameters was significantly attenuated by HF. Considering each AF level, an increase in DNA strand breaks and FPG sites with age (r = 0.655, p = 0.000, and r = 0.738, p = 0.000, respectively) was only observed in LF. Moreover, decreased mitochondrial complex I activity with age (r = −.470, p = .009) was reported in LF. These results allow the conclusion that high AF seems to play a key role in attenuating the biological aging process.     

Effects of oxidative stress on mitochondrial content and integrity of human anastomotic colorectal dehiscence: a preliminary DNA study

BACKGROUND:

Anastomotic dehiscence is one of the most severe complications of colorectal surgery. Gaining insight into the molecular mechanisms responsible for the development of anastomotic dehiscence following colorectal surgery is important for the reduction of postoperative complications.

OBJECTIVE:

Based on the close relationship between surgical stress and oxidative stress, the present study aimed to determine whether a correlation exists between increased levels of reactive oxygen species and colorectal anastomotic dehiscence.

METHODS:

Patients who underwent surgical resection for colorectal cancer were divided into three groups: patients with anastomotic dehiscence (group 1); patients without dehiscence who underwent neoadjuvant radiochemotherapy (group 2); and patients without anastomotic dehiscence who did not undergo neoadjuvant radiochemotherapy (group 3). Quantitative polymerase chain reaction and real-time polymerase chain reaction assays were performed to measure nuclear DNA and mitochondrial DNA (mtDNA) content, and possible oxidative damage to nonmalignant colon and rectal tissues adjacent to the anastomoses.

RESULTS:

mtDNA content was reduced in the colon tissue of patients in groups 1 and 2. Rectal mtDNA was found to be more damaged than colonic mtDNAs in all groups. The 4977 bp common deletion was observed in the mtDNA of tissues from both the colon and rectum of all patients.

DISCUSSION:

Patients in groups 1 and 2 were more similar to one another than to group 3, probably due to higher levels of reactive oxygen species in the mitochondria; the greater damage found in the rectum suggests that dehiscence originates primarily from the rectal area.

CONCLUSIONS:

The present study of mtDNA analyses of normal human colon and rectal tissues from patients with colorectal cancer is among the first of its kind.     

Differential expressions of antioxidant status in aging rats: the role of transcriptional factor Nrf2 and MAPK signaling pathway

Antioxidant enzymes (AOEs) play an important role in the protection of cells against reactive oxygen species and facilitate the prevention of oxidative stress-induced aging. In the present study, the antioxidant indices, including the content of peroxidation product and the expression of AOEs in rat livers of varying ages (2, 12 and 18-24 months old) were evaluated. Erythrocytes haemolysis induced by free radicals showed significant age-dependent increases (P < 0.05). The content of oxidation products in livers showed that increasing age was associated with serious oxidative injury. The activities of AOEs decreased with increasing age. Expression of the antioxidant and age-related gene, klotho, decreased with increasing age. Western blot assay showed that aged rats experience higher levels of oxidative stress. Nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) exhibited an age-dependent decrease. Additionally, the mitogen-activated protein kinase cascade (MAPK) played a regulatory role in signaling transduction. Overall, we suggest that age-related declines of the antioxidant defense are closely involved with the expression of Nrf2 and are regulated by the MAPK family.     

Effects of the association of aging and obesity on lipids, lipoproteins and oxidative stress biomarkers: A comparison of older with young men

In this study, plasma lipids, lipoproteins and markers of oxidant/antioxidant status were investigated in young (n = 45) and older (n = 40) obese men and compared to those in young (n = 65) and older (n = 55) normal weight controls. The purpose was to determine whether obesity exacerbates or not lipid, lipoprotein abnormalities and oxidative stress in older men.Our findings showed that all obese patients had increased plasma triglyceride, cholesterol, LDL-cholesterol, -triglyceride and HDL-triglyceride levels concentrations compared to controls (P < 0.01). However, the younger obese men had relatively larger and accentuated changes in plasma lipids and lipoproteins than the older patients. Additionally, total antioxidant capacity (ORAC), vitamins C and E were lower while hydroperoxides and carbonyl proteins were higher in young and older obese patients compared to their respective controls (P < 0.001). Erythrocyte antioxidant SOD and catalase activities were enhanced in obese young patients, but reduced in obese older men. Glutathione peroxidase activity was low in obesity irrespective of age. In multiple regression analysis, BMI significantly predicted total cholesterol, LDL-C, LDL-TG and HDL-TG (P < 0.0001). These relationships were not modified by age. BMI alone was a not a significant predictor for ORAC, vitamins C, E, catalase and Glutathione peroxidase. However, the interaction BMI–age significantly predicted these parameters and explained 28–45% of their changes. BMI was a significant predictor of SOD, carbonyl proteins and hydroperoxides. This effect became more significant (P < 0.0001) and worsened with BMI–age interaction.In conclusion, lipoprotein metabolism and oxidant/antioxidant status are altered in obesity irrespective of age. However, obesity-related lipid and lipoprotein alterations were attenuated while oxidative stress was aggravated in older adults.     

氧化应激在 OSAHS 所致肾损害中的作用机制及抗氧化干预的研究进展

OSAHS 是一种全身性的疾病,在其引起各系统疾病的发生发展过程中,慢性间歇低氧引起的氧化应激起着广泛的作用。本文就氧化应激在 OSAHS 所致肾损害中的作用机制及抗氧化治疗研究进展加以综述。     

Perceived stress as a risk factor for changes in health behaviour and cardiac risk profile: a longitudinal study

Objective. The aim of this study was to evaluate the long‐term effects of stress on changes in health behaviour and cardiac risk profile in men and women. Design. A prospective cohort study. Setting. The Copenhagen City Heart Study, Denmark. Subjects. The analyses were based on 7066 women and men from the second (1981–1983) and third (1991–1993) wave of the Copenhagen City Heart Study. All participants were asked questions on stress and health behaviour and they had their weight, height, blood pressure and level of blood lipids measured by trained personnel. Main outcome measures. Changes in health behaviour (smoking, physical activity, alcohol consumption, overweight) and cardiac risk profile (cholesterol, HDL cholesterol, blood pressure, diabetes). Results. Individuals with high levels of stress compared to those with low levels of stress were less likely to quit smoking (OR = 0.58; 95% CI: 0.41–0.83), more likely to become physically inactive (1.90; 1.41–2.55), less likely to stop drinking above the sensible drinking limits (0.43; 0.24–0.79), and stressed women were more likely to become overweight (1.55; 1.12–2.15) during follow‐up. Men and women with high stress were more likely to use antihypertensive medication (1.94; 1.63–2.30), and stressed men were more than two times as likely to develop diabetes during follow‐up (2.36; 1.22–4.59). Conclusion. This longitudinal study supports a causal relation between stress and cardiovascular diseases mediated through unfavourable changes in health behaviour and cardiac risk profile.     

Associations between serum homocysteine, holotranscobalamin, folate and cognition in the elderly: a longitudinal study

Abstract. Hooshmand B, Solomon A, Kåreholt I, Rusanen M, Hänninen T, Leiviskä J, Winblad B, Laatikainen T, Soininen H & Kivipelto M (Aging Research Center, Karolinska Institutet, Stockholm, Sweden; KI Alzheimer’s Disease Research Center (KI‐ADRC), Karolinska Institutet, Stockholm, Sweden; National Institute for Health and Welfare (THL), Helsinki, Finland; University of Eastern Finland, Institute of Clinical Medicine, and University Hospital, Kuopio, Finland). Associations between serum homocysteine, holotranscobalamin, folate and cognition in the elderly: a longitudinal study. J Intern Med 2012; 271 : 204–212. Objectives. To examine the associations between serum homocysteine (tHcy), holotranscobalamin (holoTC, the biologically active fraction of vitamin B12) and folate and cognitive functioning in a longitudinal population‐based study of Finnish elderly subjects. Subjects and design. tHcy, holoTC and folate were measured at baseline in 274 dementia‐free subjects aged 65–79 years from the Cardiovascular Risk Factors, Aging and Dementia study. Subjects were re‐examined 7 years later, and global cognition, episodic memory, executive functioning, verbal expression and psychomotor speed were assessed. Results. Higher baseline tHcy levels were associated with poorer performance in global cognition, relative difference: 0.90 [95% confidence interval (CI) 0.81–0.99]; episodic memory: 0.87 (95% CI 0.77–0.99); executive functions: 0.86 (95% CI 0.75–0.98); and verbal expression: 0.89 (95% CI 0.81–0.97) at follow‐up. Increased holoTC levels were related to better performance on global cognition: 1.09 (95% CI 1.00–1.19); executive functions: 1.11 (95% CI 1.01–1.21); and psychomotor speed: 1.13 (95% CI 1.01–1.26). After excluding 20 cases of incident dementia, increased tHcy remained associated with poorer performance in episodic memory, execution functions and verbal expression. Higher holoTC levels tended to be related to better performance in executive functions and psychomotor speed, while elevated serum folate concentrations were significantly related to higher scores in global cognition and verbal expression tests. Conclusions. tHcy, holoTC and folate levels are related to cognitive performance 7 years later even in nondemented elderly subjects. Randomized trials are needed to determine the impact of vitamin B12 and folate supplementation on preventing cognitive decline in the elderly.     

Analysis of gene expression during aging of CGNs in culture: implication of SLIT2 and NPY in senescence

Senescence is the major key factor that leads to the loss of neurons throughout aging. Cellular senescence is not the consequence of single cause, but there are multiple aspects which may induce senescence in a cell. Various causes such as gene expression, molecular interactions and protein processing and chromatin organization are described as causal factor for senescence. It is well known that the damage to the nuclear or mitochondrial DNA contributes to the aging either directly by inducing the apoptosis/cellular senescence or indirectly by altering cellular functions. The significant nuclear DNA damage with the age is directly associated with the continuous declining in DNA repair. The continuous decline in expression of topoisomerase 2 beta (Topo IIβ) in cultured cerebellar granule neurons over time indicated the decline in the repair of damage DNA. DNA Topo IIβ is an enzyme that is crucial for solving topological problems of DNA and thus has an important role in DNA repair. The enzyme is predominantly present in non-proliferating cells such as neurons. In this paper, we have studied the genes which were differentially expressed over time in cultured cerebellar granule neurons (CGNs) and identified potential genes associated with the senescence. Our results showed that the two genes neuropeptide Y (Npy) and Slit homolog 2 (Drosophila) (Slit2) gradually increase during aging, and upon suppression of these two genes, there was gradual increase in cell viability along with restoration of the expression of Topo IIβ and potential repair proteins.

Graphical abstract

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一种新发现的线粒体DNA大片段缺失与衰老的关系初探

目的 在人外周血细胞中筛选新的线粒体DNA（mtDNA）大片段缺失突变,探讨mtDNA尤其在片段缺失突变与衰老的关系。方法 以人外周血细胞DNA为模板,进行聚合酶链反应（PCR）扩增,产物克隆、测序。用PCR半定量方法测定1条长达13．1kb的mtDNA缺失突变,＜60岁组和≥60岁组突变型与野生型的比例,差异有显著性。结论 该突变以前未见报道,可能是一种与衰老有关的缺失突变。