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PubMed1982

Photoreactivation in two closely related marine fishes having different longevities.

The tautog, Tautoga onitis, and cunner, Tautogolabrus adspersus, are marine fishes which are closely related taxonomically (family Labridae), have similar habits, the same ecological requirements and are found in the same areas. However, they differ markedly in their longevity. The tautog is longer-lived, reaching an estimated average age of 34 years. It attains sexual maturity at 3--4 years of age. The cunner, on the other hand, lives to about 5--6 years of age and is sexually mature at about one year. An examination of their respective capacities for photoreactivation using cells in tissue culture derived from these fishes revealed marked differences in the rate of monomerization of ultraviolet-induced pyrimidine dimers from their DNA. Radiochromatographic analysis of dimers in the tautog showed that half the dimers were removed within a period of 10 min of exposure to photoreactivating light whereas a 50-min exposure was required to photoreactivate dimers to this same level in the cunner. Dark repair of dimers was measured by radiochromatography and by endonuclease assay. The two methods showed similar low levels of excision repair in both species.

Animals↗
PubMedDate not supplied

Selection of conidial longevity mutants of Neurospora crassa.

Conidial survival was measured after incubation in white light at 30 degrees C and 85-100% relative humidity. The heritable median lifespan (MLS) of the wild-type ( age0 ) was 22 days. Spontaneous short-lived mutants (age-) with MLS about 7 days occurred among both sexual and asexual progeny of wild-type at a frequency of about 10%. Radiation of conidia with near ultraviolet light increased the mutation frequency about 5-9-fold above spontaneous. The apparent spontaneous reversion frequency was about 0.1% or less. Four lines of evidence indicated that conditional defective conidiophorogenesis is a pleiotropic expression of the age- mutations. Of five age- mutants tested, all were photosensitive and remedial by vitamin E, exhibiting wild-type survival in darkness or after preculture with vitamin E. Selective breeding yielded variants (age+) with about 14-day increments of MLS at each of three generations beyond the F1. The segregation of either age- or age+ in crosses to age0 was Mendelian. A survey of mutants of 61 genes with other biochemical or morphological phenotypes indicated, as a conservative estimate, that 9 or 15% may exert a pleiotropic adverse effect on conidial longevity.

Chromosome Mapping↗
PubMedDate not supplied

Linkage of conidial longevity determinant genes in Neurospora crassa.

The longevity of conidia of Neurospora crassa was previously defined as their ability to grow after aging in a constant environment. The heritable median lifespan of the wild type is 22 days. Heritable mutants with lifespans of 5-7 days were previously selected. The pleiotropic colony phenotype of the mutants greatly facilitates genetical analysis of their inheritance. Twenty-eight mutants were mapped by recombinational analysis. All but one were located at genes on one arm of the seven chromosomes, linkage group IR; the exception was at the terminus of linkage group VIR. Sixteen of the 17 genes on IR are collectively called the age-1 complex. The average and standard deviation of the distance of 13 intervals between adjacent genes in the complex was 4.9 +/- 1.1 map units; hence they appear to be spatially reiterated. Other observations indicate that the genes are also functionally redundant.

Chromosome Mapping↗
PubMed1986

Interaction of H-2 genotype and basal serum immunoglobulin A level influences longevity.

The congenic pair of mice, C57BL/10 (B10) and C57BL/10.F (B10.F), differ at the H-2 locus and have mean ages at death of 706 and 456 days, respectively. B10.F also has reduced basal serum IgA levels compared with B10, 63 and 256 mg/dl, respectively. Controlled matings between the two strains of mice were used to identify genetic factors that govern longevity. F2 and backcross progeny from reciprocal F1 hybrids were classified for H-2 genotype and serum IgA levels and allowed to live out their lifespan. F2 and backcross progeny homozygous for the H-2 allele of B10.F had a mean age at death (602 days) significantly reduced from that of progeny homozygous for the H-2 allele of B10 (689 days). However, the greatest reduction of lifespan occurred among progeny of the (B10.F X B10)F1 mothers, 693 compared with 540 days. The strain of the maternal parent also has been shown to affect the segregation of IgA phenotypes. An increased incidence of low IgA phenotype associated with H-2 genotype was observed among progeny of (B10.F X B10)F1 mothers. Survival curves demonstrated a relationship between low serum IgA levels and shortened lifespan and no maternal effect was observed. The basis of the shortened lifespan among progeny of F1 hybrids in which the maternal parent was B10.F was the increased incidence of offspring with low IgA phenotypes. The apparent association of H-2 and shortened lifespan also was because the low IgA phenotype was more frequent among progeny that carried the H-2 allele of the B10.F strain. The B10.F mice spontaneously shed an endogenous ecotropic retrovirus which may be responsible for the maternal effect on immunoglobulin levels and lifespan.

Animals↗
PubMed1987

Cellular aging (the Hayflick limit) and species longevity: a unification model based on clonal succession.

A model is presented which proposes a specific cause-and-effect relationship between a limited cell division potential and the maximum lifespan of humans and other mammals. It is based on the clonal succession hypothesis of Kay which states that continually replicating cell beds (e.g. bone marrow, intestinal crypts, epidermis) could be composed of cells with short, well-defined division potentials. In this model, the cells of these beds are proposed to exist in an ordered hierarchy which establishes a specific sequence for cell divisions throughout the organism's lifespan. The depletion of division potential at all hierarchical levels leads to a loss of bed function and sets an intrinsic limit to species longevity. A specific hierarchy for cell proliferation is defined which allows the calculation of time to bed depletion and, ultimately, to organism mortality. The model allows the existence of a small number (n) of critical cell beds within the organism and defines organism death as the inability of any one of these beds to produce cells. The model is consistent with all major observations related to cellular and organismic aging. In particular, it links the PDLs (population doubling limit) observed for various species to their mean lifespan; it explains the slow decline in PDL as a function of age of the donor; it establishes a thermodynamically stable maximum lifespan for a disease-free population; and it can explain why tissue transplants outlive donors or hosts.

Aging↗
PubMed1988

Effect of lifetime administration of dimethylaminoethanol on longevity, aging changes, and cryptogenic neoplasms in C3H mice.

The effects of lifetime treatment with dimethylaminoethanol on longevity and cryptogenic neoplasm formation were studied in females of two mouse sub-lines, the C3H/HeN which carries a germinal mammary tumor provirus and the C3H/HeJ(+) which also carries the exogenous mammary tumor virus. Administration in the drinking water of 10 mM dimethylaminoethanol to the C3H/HeN mice or 15 mM to the C3H/HeJ(+) mice did not result in significant differences between treated and untreated groups in average survival. No changes in age-related organ structure or morphology were observed with dimethylaminoethanol treatment, except for an apparent decrease in the amount of lipofuscin in the liver judged in histological sections. Among untreated C3H/HeJ(+) females, 89% developed neoplasms of the mammary gland, ovary, liver, lung and reticuloendothelial system, while the incidence was 88% in the treated mice. In C3H/HeN females, neoplasms of the mammary gland, ovary, liver, lung and lymphatic system occurred in 57% and in 60% of treated mice. Also, there was no statistically significant difference between control and treated animals in the age of onset or the type of specific neoplasms. Dimethylaminoethanol did not induce any neoplasms.

Aging↗
PubMed1993

A monogenic senility syndrome segregating with longevity in mice.

We have found that around 2 years of age all surviving CBA T6/T6 mice develop hyperactivity and progressive weight loss, terminating in death, which is preceded in the males by priapism, persistent penile erection. As there is no genital lesion, the priapism is presumably of neurogenic origin, providing an invaluably specific sign of development of a neurological lesion. A loss of neurons, somewhere in the brain stem, not detectable without computerised, automated microscopy, not yet applied, is at present the best explanation for the occurrence of the syndrome. In maternally-derived F2 hybrids with the NZW and C57 BL/6 strains, the syndrome occurs exactly as in the CBAs, with a frequency of 25%, indicative of mediation by a single gene or gene cluster. The syndrome also occurs in the F1 hybrids, but with a 34-week delay, suggesting a delaying effect of either a halved CBA gene dosage, or of non-CBA genes. In NZW F2 hybrids the syndrome segregates with longevity (P < 0.001). The phenomenon provides an animal model for study of mechanisms of ageing and their relationship to senile neuropathies, such as Alzheimer's disease.

Aging↗
PubMed1993

Comparison of mitochondrial pro-oxidant generation and anti-oxidant defenses between rat and pigeon: possible basis of variation in longevity and metabolic potential.

Non-passerine birds and mammals of similar body weight have a roughly comparable metabolic rate, but the life span and the metabolic potential, i.e. the total amount of energy consumed per unit of body mass during life, is several times higher in the birds. The objective of this study was to explore the possible basis of this characteristic in the context of the predictions of the free radical hypothesis of aging. Accordingly, pigeon and rat, which have a similar body weight, were compared by examining the mitochondrial rates of O2.- and H2O2 generation and activities of superoxide dismutase, catalase and glutathione peroxidase and concentration of glutathione in the brain, heart and kidney. Compared with the rat, the rate of mitochondrial O2.- generation in the pigeon ranged between 50 and 67%, and H2O2 production between 31 and 77%. Activity of superoxide dismutase was uniformly higher and catalase activity consistently lower in the tissues of the pigeon compared with the rat. Glutathione peroxidase activity and glutathione concentration were higher in the pigeon in two out of the three organs studied, and comparable in the third organ. The magnitude of the differences between the two species was greater in the rates of O2.- and H2O2 generation than in anti-oxidant defenses. Results indicate that the relatively greater longevity and metabolic potential of the pigeon may be related to significantly lower rates of O2.- and H2O2 generation and higher overall level of anti-oxidant defenses.

Animals↗
PubMed1995

Strain, stress, neurodegeneration and longevity.

Laboratory studies indicate that the life-span of inbred rodent strains is inversely related to the intensity of their behavioral and neuroendocrine responses to stressful stimuli. In the brain, a shorter life-span is associated with accelerated age-dependent degenerative changes in specific stress-responsive neuronal systems. The evidence suggests a possible genetic linkage between the intensity of the stress response, the rate of age-dependent neurodegeneration and the individual's life expectancy. It is proposed that inherent hyper-reactivity to stressors is genetically linked to a shorter life-span and to accelerated age-dependent neurodegeneration. Several experimental approaches to test 'this stress-longevity-neurodegeneration linkage hypothesis' are outlined.

Aging↗
PubMed1985

Effect of exercise on longevity, body weight, locomotor performance, and passive-avoidance memory of C57BL/6J mice.

Studies of human and animal subjects have suggested that exercise may retard aging, help prevent age-related diseases, and prolong life span. Earlier studies focused on the effects of exercise on the heart, skeletal muscles, lungs, metabolism, and longevity. Researchers recently have begun to direct their attention to possible benefits of exercise on the brain. The goals of this study were to examine the effects of voluntary wheel-running exercise on life span, body weight, food and water intake, locomotor performance, and one-trial passive-avoidance memory of mature (10-14 month), middle-aged (20-24 month), and old (28-30 month) C57BL/6J male mice. No significant differences in life span, expressed in months, were found between control and exercised mice when exercise was carried out during maturity, senescence, intermittently across both periods, or continuously throughout maturity and senescence. Exercised adult mice maintained body weight compared to adult controls, an effect not apparent in old mice. Locomotor performance was reduced in old mice, and exercise increased performance much more in adult than in old mice. In the passive avoidance test of recent memory, exercise significantly increased latency, that is, it improved retention, in adult, middle-aged, and old mice. The effect was greatest in middle-aged, next in old, and lowest in adult mice. The findings indicate that exercise may be an important modulator of the rate of aging.

Aging↗
PubMedDate not supplied

The effect of increased longevity, produced by dietary restriction, on the neuronal population of area 17 in rat cerebral cortex.

Area 17 of the brains of Sprague-Dawley derived rats, maintained on a limited ration of food to maintain their weights at the levels attained by two months of age, was compared with area 17 in control groups of rats fed ad lib. The oldest rats in the diet restricted group were sacrificed at 46 and 48 months of age, by which time their life spans had been extended about 12 months beyond the oldest age that rats fed ad lib achieve, for only few of the latter live as long as 33 months. In this study, the rats which were compared consisted of two groups of ad lib fed rats, one 3 and 6 months of age, and the other 33 months old, and two groups of diet restricted rats, one 26 months old and the other 46 to 48 month old rats (designated as 47 month old rats). Two indices were used to assess whether age affects the volume of area 17. One, the number of clusters of apical dendrites of layer V pyramidal cells per unit area of tangential sections, was the same in all groups, indicating that the lateral spread of area 17 did not alter with age. However, the other index, the thickness of area 17, did change with age, for area 17 was significantly thinner in the 47 month old diet restricted rats than in the other three groups. It was also found that the number of neuronal profiles in strips of sections passing through the entire depth of area 17 is decreased in the 47 month old rats, indicating that neurons had been lost from their cortices. This decrease in the number of neuronal profiles in the 47 month old rats was not due to nuclear shrinkage since the sizes of neuronal nuclei were not significantly different in the older ad lib and diet restricted rats. Determinations of neuronal packing densities in layers II/III, IV, V and VIa suggest that neurons are most frequently lost from the deeper cortical layers of the 47 month old rats, and in these layers large vacuolated spaces, the sizes of neuronal cell bodies, have been encountered. It is suggested that these spaces represent places from which neurons have been lost. It is concluded, therefore, that neurons are lost from area 17 in rats whose longevity is increased by diet restriction.

Animals↗
PubMed1982

Population genetic models in the study of aging and longevity in a Mennonite community.

This is a preliminary report on a 3-year multidisciplinary study of aging among historically and genetically related Mennonite congregations in Kansas and Nebraska. Three aspects of longevity and aging are examined: (1) the relationship of heterozygosity to survivorship using 8 genetic blood group loci, (2) changes in taste sensitivity with age using 14 dilutions of PTC; and (3) life span correlations among parents and offspring during a 100 year period. Heterozygosity was found to be independent of survivorship. No diminution in taste sensitivity to PTC was found with increasing age although a significant difference in PTC taste thresholds was found between males and females. No relationship was found between nontasters and individuals with a history of thyroid disease. Mother's life span was found to correlate more closely with daughter than any other familial correlation.

Adolescent↗
PubMed1991

Social networks and longevity. A 14 year follow-up study among elderly in Denmark.

The hypothesis of the study was that social contacts to close friends and relatives and perceived social integration was able to delay mortality in general and cardiovascular mortality in particular. Altogether 1752 males and females, aged 70-100 years were interviewed by trained nurses in 1972 to 1974. The study group was based upon a random sample of all elderly in the town of Odense, Denmark. More than 80% participated in the survey which included data collection on social networks and health at the time of interviewing. By means of linking the study group to national registries on mortality and causes of mortality practically all in the cohort were traced until 1987. During follow-up 1501 persons died. Most of the association between social networks and mortality were weak and statistically insignificant but had the expected sign. After adjusting for initial health status only the interviewer's assessment of the quality of the network was statistically significant associated with longevity. A feeling of loneliness was found to be associated with cardiovascular mortality, especially for males.

Aged↗
PubMed1990

Influence of food intake and sexual segregation on longevity, organ weights and the incidence of non-neoplastic and neoplastic diseases in rats.

In a small-scale experiment the effects of four variables were investigated in male and female Wistar rats fed on a standard laboratory chow and not deliberately exposed to any carcinogen. The variables investigated were (i) diet restriction by limiting access to food to 6.5 hr/day instead of 24 hr/day; (ii) housing males in a single-sex room as distinct from a mixed-sex room; (iii) life-long segregation of males from females, as distinct from access to one virgin female for 5 days during each alternate week; and (iv) uniparity in females versus life-long virginity. The endpoints compared were body-weight gain, longevity, visible and palpable swellings, absolute and relative organ weights, microscopically confirmed malignant neoplasms that contributed to death before the end of the study at 2 yr, incidence of other neoplasms in decedents and rats killed at the end of the study, and the incidence of various non-neoplastic conditions including myocardial inflammation and fibrosis, chronic progressive nephropathy, liver glycogen storage and fatty degeneration, mammary gland hyperplasia and secretory activity, pancreatic polyarteritis, radiculoneuropathy and certain testicular changes. The results indicated major beneficial effects of dietary restriction on most of the endpoints. By comparison the other variables had only marginal effects. Leydig-cell hyperplasia and neoplasia occurred at significantly higher incidences in males housed intermittently with females than in permanently segregated males. No convincing differences were seen between females that littered once and those that remained virgins. The relevance of these findings to the prediction of cancer mortality risk in man and to the design of rodent carcinogenicity studies is discussed.

Animals↗
PubMed1980

The evolution of human longevity.

In the comparatively short history of human evolution man's lifespan has doubled, posing the question, by what means was this prolongation of life achieved. One line of thought correlates lifespan with oxygen consumption and energy generation, pointing out that small homeothersms which expend energy at a very high rate, are invariable short lived, while animals living more economically in terms of energy expenditure, like some heterotherms and large homeotherms, can attain greatly increased lifespan potentials. The correlation between lifespan and energy expenditure is generally valid, but some animals with low energy needs, notably tropical animals and some lethargic, inactive animals, do not live as long as expected on the basis of the theory. The present paper suggest that the aging process could be accelerated by hyperthermia and the longevity of some homeotherms, beside its connection with energy needs, could also be correlated with the evolution of temperature regulating mechanisms, resulting in more accurate thermal homeostasis. Man's uniquely capacious sweating mechanism, for example, may play a part in the attainment of his long life.

Aging↗
PubMed1982

Maternal age and lifespan do not influence longevity in the rotifer Asplanchna brightwelli.

An analysis of the mean lifespans among the progeny of the viviparous rotifer Asplanchna brightwelli produced during four generations has revealed that longevity of the offspring is not affected by maternal age of the parent or by the parent's lifespan. The production of viable offspring at any time during the parent's reproductive period may be of importance in assuring the continuity of clones of this short-lived rotifer species.

Animals↗
PubMed1983

Resource availability, maternal effects, and longevity.

Experiments with a clone of the cladoceran Daphnia pulex indicate that the nutritional conditions of the maternal environment play a major role in determining the progeny's phenotype. Apparently, by influencing the physiology and/or morphology of individuals during early development, maternal investment not only enhances juvenile survival but has long-lasting, favorable effects on the progeny's ability to convert resources into growth and reproduction as well as negative repercussions for adult survival of the progeny. Life-span may also be radically altered by modifying food schedules within an individual's life. Neither reproductive effort nor rate of living hypotheses can explain longevity variation within Daphnia clones; rather the onset of senescence appears to be associated with a general breakdown in the ability to incorporate energy into biomass. Analysis of our results as well as earlier data with a "rate of aging-threshold vitality" model suggests that increasing the availability of food to an individual increases the rate of aging while decreasing the threshold vitality necessary for survival and that increasing maternal investment increases both the vitality at birth and the rate of aging of the progeny.

Animals↗
PubMed1987

The rate of living theory. Spontaneous locomotor activity, aging and longevity in Drosophila melanogaster.

The spontaneous locomotor activity (SLA) of 50 males and 50 females of Drosophila melanogaster has been recorded over a 12-h photophase once a week throughout their entire life span. In females, the SLA score regularly decreases with age. In males, the SLA score increases up to the 5th week of age and then decreases. In each sex, the correlation between the mean level of SLA displayed by the flies during their life and longevity was not significant. Less active flies are not the long-lived ones. This result is not in accordance with the rate of living theory.

Aging↗