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Holmes DJ, Flückiger R, Austad SN. Comparative biology of aging in birds: an update. Exp Gerontol. 2001 Apr; 36(4-6):869-83.
... In spite of their relatively high metabolic rate, body temperature, and blood glucose-factors that contribute to decreased lifespan in mammals-birds appear to have physiological advantages that allow them to live up to three times longer than mammals of equivalent sizes (Austad, 1997;Holmes, Flückiger, & Austad, 2001). Because of their relatively long lifespan and successful adaptations to aging compared with laboratory rodents, avian species may be promising for modeling resilience to senescence. ...
... utilize laboratory rats and mice, which are relatively small and short-lived mammalian species. Whereas body size and longevity generally correlate in mammals, this is not the case in birds; birds generally live up to three times longer than do mammals of a similar size (Holmes & Austad, 1995;Holmes et al., 2001;Holmes & Ottinger, 2003). Captive mice, for example, live for up to 4 years, whereas a comparably sized captive songbird, the zebra finch, lives up to 9 years (Holmes & Ottinger, 2003). ...
... Captive mice, for example, live for up to 4 years, whereas a comparably sized captive songbird, the zebra finch, lives up to 9 years (Holmes & Ottinger, 2003). Though birds are susceptible to diseases and injuries that afflict mammals, they demonstrate relatively lower rates of physiological decline (Holmes & Austad, 1995;Holmes et al., 2001;Holmes & Ottinger, 2003;Munshi-South & Wilkinson, 2010). Therefore, zebra finches may make excellent models for human longevity and offer insight into the mechanisms of senescence and successful aging. ...
Age-related decrements in cognitive ability have been proposed to stem from deteriorating function of the hippocampus. Many birds are long lived, especially for their relatively small body mass and elevated metabolism, making them a unique model of resilience to aging. Nevertheless, little is known about avian age-related changes in cognition and hippocampal physiology. We studied spatial cognition and hippocampal expression of the age-related gene, Apolipoprotein D ( ApoD ), and the immediate early gene Egr-1 in zebra finches at various developmental time points. In a first experiment, middle-aged adult males outperformed middle-aged females in learning correct food locations in a four-arm maze, but all birds remembered the task equally well after a 5- or 10-day delay. In a second experiment comparing young and old birds, aged birds showed minimal evidence for deterioration in spatial cognition or motivation relative to young birds, except that aged females showed less rapid gains in accuracy during spatial learning than young females. These findings indicate that sex differences in hippocampus-dependent spatial learning and decline with age are phylogenetically conserved. With respect to hippocampal gene expression, adult females expressed Egr-1 at significantly greater levels than males after memory retrieval, perhaps reflecting a neurobiological compensation. Contrary to mammals, ApoD expression was elevated in young zebra finches compared with aged birds. This may explain the near absence of decrements in spatial memory due to age, possibly indicating an alternative mechanism of managing oxidative stress in aged birds.
... mole-rat has extreme longevity compared with other rodents of similar size, despite a high level of free radicals and significant levels of oxidative damage in proteins, lipids and DNAs [16][17][18][19]. Second, variations in LEE in mammals and birds exhibit diverse distribution patterns [20]. On the basis of these observations, researchers have argued that the rate-of-living theory cannot be correct, MLS is not a good marker of ageing, BMR is not a good measure of total energy metabolism [21] and reactive oxygen species are not causally linked with ageing [6,8]. ...
... Recent structural studies on MMPs have shown that the respiratory chain has a high degree of sequence conservation in the membrane integral central subunits [50]; therefore, its mechanism is likely to be similar across species [37]. However, we recently demonstrated that the four AAVs of SC, TC, CC and HYD of MMPs are highly variable across species and can be related to MLS [20,27]. A significant correlation between CC and MLS in metazoans has also been reported [25,47]. ...
Current ageing theories are far from satisfactory because of the many determinants involved in ageing. The well-known rate-of-living theory assumes that the product (lifetime energy expenditure, LEE) of maximum lifespan (MLS) and mass-specific basal metabolic rate (msBMR) is approximately constant. Although this theory provides a significant inverse correlation between msBMR and MLS as a whole for mammals, it remains problematic for two reasons. First, several interspecies studies within respective orders (typically within rodents) have shown no inverse relationships between msBMR and MLS. Second, LEE values widely vary in mammals and birds. Here, to solve these two problems, we introduced a new quantity designated as mitochondrial (mt) lifetime energy output, mtLEO = MLS × mtMR, in place of LEE, by using the mt metabolic rate (mtMR) per mitochondrion. Thereby, we found that mtLEO values were distributed more narrowly than LEE ones, and strongly correlated with the four amino-acid variables (AAVs) of Ser, Thr and Cys contents and hydrophobicity of mtDNA-encoded membrane proteins (these variables were related to the stability of these proteins). Consequently, only these two mt items, mtMR and the AAVs, solved the above-mentioned problems in the rate-of-living theory, and thus extensively improved the correlation with MLS compared with that given by LEE.
... However, the connections between the elements of the network are more complex than initially assumed. For instance, birds live longer than mammals of comparable mass, yet have a faster rate of metabolism (Holmes et al. 2001). Shorter lifetime and faster metabolism are also not always correlated with a higher rate of H 2 O 2 production (Barja Gustavo 1998;Law et al. 2016), and telomere length or telomerase activity cannot be always used as lifespan predictors. ...
Studies on human telomeres have established that telomeres exert a significant influence on lifespan and health of organisms. However, recent research has indicated that the original idea that telomeres affect lifespan in a universal and central manner across all eukaryotic species is an oversimplification. Indeed, findings from a variety of animal species revealed that the role of telomere biology in aging is more subtle and intricate than previously recognized. Here, we show how telomere biology varies depending on the taxon. We also show how telomere biology corresponds to basic life history traits and affects the life table of a species and investments in growth, body size, reproduction, and lifespan; telomeres are hypothesized to shape evolutionary perspectives for species in an active but complex manner. Our evaluation is based on telomere biology data from many examples from throughout the animal kingdom that vary according to the degree of organismal complexity and life history strategies.
Attack by reactive oxygen intermediates, common to many kinds of cell/tissue injury, has been implicated in the development of diabetic and other vascular diseases. Such oxygen-free radicals can be generated by advanced glycation end products (AGEs), which are nonenzymatically glycated and oxidized proteins. Since cellular interactions of AGEs are mediated by specific cellular binding proteins, receptor for AGE (RAGE) and the lactoferrin-like polypeptide (LF-L), we tested the hypothesis that AGE ligands tethered to the complex of RAGE and LF-L could induce oxidant stress. AGE albumin or AGEs immunoisolated from diabetic plasma resulted in induction of endothelial cell (EC) oxidant stress, including the generation of thiobarbituric acid reactive substances (TBARS) and resulted in the activation of NF-kappaB, each of which was blocked by antibodies to AGE receptor polypeptides and by antioxidants. Infusion of AGE albumin into normal animals led to the appearance of malondialdehyde determinants in the vessel wall and increased TBARS in the tissues, activation of NF-kappaB, and induction of heme oxygenase mRNA. AGE-induced oxidant stress was inhibited by pretreatment of animals with either antibodies to the AGE receptor/binding proteins or antioxidants. These data indicate that interaction of AGEs with cellular targets, such as ECs, leads to oxidant stress resulting in changes in gene expression and other cellular properties, potentially contributing to the development of vascular lesions. Further studies will be required to dissect whether oxidant stress occurs on the cell surface or at an intracellular locus.
Although many studies report a difference in reproductive success between old and young birds, little is known about how, why and when productivity changes as individuals age. We examined age-dependent reproduction in two bird species that inhabit harsh tundra environments: White-tailed Ptarmigan Lagopus leucurus in alpine areas and Willow Ptarmigan Lagopus lagopus in subarctic Canada. We evaluated reproductive performance in the light of three hypotheses: constraint, restraint and selection. Using cross-sectional and longitudinal data, we observed significant age effects in seven of the eight life history and behavioural traits examined for the two species. However, the pattern of age effects variedconsiderably across life history stages; younger birds generally had smaller clutches, later laying dates and poorer spring body condition, but the nesting success did not vary with age. Brood-rearing and renesting abilities were greater for older parents. The oldest age class of White-tailed Ptarmigan showed reproductive senescence for laying date and clutch size but fledged such a large proportion of the brood that they had the highest overall production of any class. It thus appears that parental experience can compensate for reduced physical ability to produce eggs. Annual mortality rates for breeding females were U-shaped for White-tailed Ptarmigan, with higher rates for young and old birds, but mortality did not change with age in Willow Ptarmigan. Overall, the two species differed in the presence of age dependence for only two traits (renesting ability and annual survival). Age-dependent effects were generally greater for White-tailed Ptarmigan than for Willow Ptarmigan. The patterns of mortality and fecundity we observed in ptarmigan provide general support for the constraint hypothesis of reproductive performance. By examining discrete stages of reproduction, we identified the life history stages where age effects occur and propose proximate mechanisms responsible for these effects.
SENESCENCE is the innate deterioration of an organism that leads to a decline in its fitness components such as fecundity and survival expectations with advancing age1,2. Williams3 proposed that the evolution of senescence could be understood in terms of age-specific pleiotropic gene action, where a mutation increases fitness early in life at the expense of reducing it later on. The basic idea, first proposed by Medawar1, is that mutations acting early in life are more sensitive to selection than those acting later, as the early effects would be expressed in more individuals than would the late effects. A cost of reproduction, where an increase in reproductive rate reduces future survival or fecundity, could be the kind of pleiotropic gene action that generates senescence2,3. Evidence exists for such costs in animals and plants4-8, but their role in the evolution of senescence is so far not clear2. Most empirical work has been with fruit-flies in laboratory studies, where selection experiments indicate negative genetic correlations between early and late fitness components9-12. But it is not certain how applicable the results of such studies are to natural populations. Here we report that the clutch size of older individuals in the collared flycatcher Ficedula albicollis is affected by their reproductive effort early in life. This provides empirical support for Williams's idea that costly reproduction accelerates senescence for fertility in a vertebrate species under natural conditions.
SYNOPSIS. The long life spans of birds relative to those of mammals are intriguing to biogerontologists, particularly in light of birds' high body temperatures, high blood glucose levels, and high metabolic rates—all of which should theoretically increase their biochemical liability for rapid aging. The comparative longevity of birds and other flying homeotherms is consistent with evolutionary senescence theory, which posits that species with low mortality rates from predation or accident will be released from selection for rapid maturity and early reproduction, and will exhibit retarded aging. Comparative analyses of avian life history parameters to date, although not as extensive as those for mammals, broadly support an association between low mortality rates, slow reproduction, and long lifespan. The diversity of bird life histories suggests the importance of developing a diversity of avian models for studies of aging mechanisms, both proximate and ultimate, and for using wild as well as domestic representatives. Birds studied in the laboratory thus far show many of the same manifestations of aging as mammals, including humans, and many ornithologists are beginning to document actuarial evidence consistent with aging in their study populations. We encourage greater communication and collaboration among comparative gerontologists and ornithologists, in the hope that the study of aging in birds will lead to an integrated understanding of physiological aging processes well grounded in an evolutionary paradigm.
California gulls ( Larus californicus ) of known age and sex were censused on their breeding colony in 1979, 1980 and 1984 through 1993. Ages of 235 males and 196 females ranged from 4 to 27 years. Age classes used in the analysis were limited to 17, 4 through 19, and 20 or more as a final age category because data on gulls over 20 were sparse. Survival declined with age in a way that was parsimoniously modelled with a quadratic function. Other factors, sex and time, did not explain any variation in survival. Resighting depended on age, sex and time. Younger adults skipped breeding more frequently than did older adults, and females skipped breeding more frequently than did males. There was also good evidence for time dependence in resighting probability, but its inclusion in the model occurred at the expense of interpretability and precision. In a data set such as this, resighting probability may assume more importance than a mere 'nuisance parameter'. In this study, resighting history measured attendance at the breeding ground. In turn, attendance rates may be a manifestation of reproductive strategy, which can also have consequences for survival. In this situation, there may be heterogeneity in both survival and resighting probability that is unexplained by the model. While such complexity may well be a nuisance to deal with, it can also point to important biological questions.
A fluorescent compound has been detected in proteins browned during Maillard reactions with glucose in vitro and shown to be identical to pentosidine, a pentose-derived fluorescent cross-link formed between arginine and lysine residues in collagen (Sell, D. R., and Monnier, V. M. (1989) J. Biol. Chem. 264, 21597-21602). Pentosidine was the major fluorophore formed during nonenzymatic browning of ribonuclease and lysozyme by glucose, but accounted for less than 1% of non-disulfide cross-links in protein dimers formed during the reaction. Pentosidine was formed in greatest yields in reactions of pentoses with lysine and arginine in model systems but was also formed from glucose, fructose, ascorbate, Amadori compounds, 3-deoxyglucosone, and other sugars. Pentosidine was not formed from peroxidized polyunsaturated fatty acids or malondialdehyde. Its formation from carbohydrates was inhibited under nitrogen or anaerobic conditions and by aminoguanidine, an inhibitor of advanced glycation and browning reactions. Pentosidine was detected in human lens proteins, where its concentration increased gradually with age, but it did not exceed trace concentrations (less than or equal to 5 mumol/mol lysine), even in the 80-year-old lens. Although its precise carbohydrate source in vivo is uncertain and it is present in only trace concentrations in tissue proteins, pentosidine appears to be a useful biomarker for assessing cumulative damage to proteins by nonenzymatic browning reactions with carbohydrates.
Pentosidine is a recently discovered fluorescent protein cross-link from human extracellular matrix that involves lysyl and arginyl residues in an imidazo (4, 5b) pyridinium ring. Pentosidine could be synthesized in vitro by the reaction of ribose, lysine, and arginine. The potential biological significance of the molecule prompted us to investigate its mechanism of formation from D-ribose and key Maillard intermediates, as well as from other potential precursor sugars. The yield of pentosidine from N alpha-t-Boc-lysine, N alpha-t-Boc-arginine, and D-ribose was highest at pH 9.0 and 65 degrees C, but was unaffected by reactant ratios at alkaline pH suggesting an important role for base catalysis. Ribated Boc-lysine on incubation with N alpha-t-Boc-arginine afforded a fluorescent compound with UV, fluorescence, 1H NMR, and MS properties identical with those from native or synthetic pentosidine. 3-Deoxypentosone, however, was not a major pentosidine precursor. Pentosidine became slowly detectable in bovine serum albumin incubated with 0.25 M and 1.0 M glucose and reached, at 30 days, 13.2 and 17 pmol/mg bovine serum albumin, respectively. Spectroscopical properties of glucose-derived pentosidine were identical with those from ribose-derived pentosidine. Pentosidine formed from glucated Boc-lysine with N alpha-t-Boc-arginine in higher yields than from glucose under standard conditions. Fructose, and unexpectedly ascorbate, also formed pentosidine in similar yields as glucose. The discovery that pentosidine can form not only from pentoses but also from hexoses and ascorbate raises major new questions concerning biochemical pathways of the Maillard reaction in vivo.
The chemistry of Maillard or browning reactions of glycated proteins was studied using the model compound, N alpha-formyl-N epsilon-fructoselysine (fFL), an analog of glycated lysine residues in protein. Incubation of fFL (15 mM) at physiological pH and temperature in 0.2 M phosphate buffer resulted in formation of N epsilon-carboxymethyllysine (CML) in about 40% yield after 15 days. CML was formed by oxidative cleavage of fFL between C-2 and C-3 of the carbohydrate chain and erythronic acid (EA) was identified as the split product formed in the reaction. Neither CML nor EA was formed from fFL under a nitrogen atmosphere. The rate of formation of CML was dependent on phosphate concentration in the incubation mixture and the reaction was shown to occur by a free radical mechanism. CML was also identified by amino acid analysis in hydrolysates of both poly-L-lysine and bovine pancreatic ribonuclease glycated in phosphate buffer under air. CML was also detected in human lens proteins and tissue collagens by HPLC and the identification was confirmed by gas chromatography/mass spectroscopy. The presence of both CML and EA in human urine suggests that they are formed by degradation of glycated proteins in vivo. The browning of fFL incubation mixtures proceeded to a greater extent under a nitrogen versus an air atmosphere, suggesting that oxidative degradation of Amadori adducts to form CML may limit the browning reactions of glycated proteins. Since the reaction products, CML and EA, are relatively inert, both chemically and metabolically, oxidative cleavage of Amadori adducts may have a role in limiting the consequences of protein glycation in the body.
Birds are unique since they can combine a high rate of oxygen consumption at rest with a high maximum life span (MLSP). The reasons for this capacity are unknown. A similar situation is present in primates including humans which show MLSPs higher than predicted from their rates of O2 consumption. In this work rates of oxygen radical production and O2 consumption by mitochondria were compared between adult male rats (MLSP = 4 years) and adult pigeons (MLSP = 35 years), animals of similar body size. Both the O2 consumption of the whole animal at rest and the O2 consumption of brain, lung and liver mitochondria were higher in the pigeon than in the rat. Nevertheless, mitochondrial free radical production was 2-4 times lower in pigeon than in rat tissues. This is possible because pigeon mitochondria show a rate of free radical production per unit O2 consumed one order of magnitude lower than rat mitochondria: bird mitochondria show a lower free radical leak at the respiratory chain. This result, described here for the first time, can possibly explain the capacity of birds to simultaneously increase maximum longevity and basal metabolic rate. It also suggests that the main factor relating oxidative stress to aging and longevity is not the rate of oxygen consumption but the rate of oxygen radical production. Previous inconsistencies of the rate of living theory of aging can be explained by a free radical theory of aging which focuses on the rate of oxygen radical production and on local damage to targets relevant for aging situated near the places where free radicals are continuously generated.
Cooperative breeding is an unusual kind of social behaviour, found in a few hundred species worldwide, in which individuals other than the parents help raise young. Understanding the apparently altruistic behaviour of helpers has provided numerous challenges to evolutionary biologists. This book includes detailed first-hand summaries of many of the major empirical studies of cooperatively breeding birds. It provides comparative information on the demography, social behaviour and behavioural ecology of these unusual species and explores the diversity of ideas and the controversies which have developed in this field. The studies are all long-term and consequently the book summarises some of the most extensive studies of the behaviour of marked individuals ever undertaken. Graduate students and research workers in ornithology, sociobiology, behavioural ecology and evolutionary biology will find much of value in this book.
When strong positive heritability of fitness arises due to host-parasite coevolution, consequent sosigonic mate preference undermines monogamy through tendencies to extra-pair copulation. "Low' females bonded to "low' males try to parasitise their partnership by obtaining fertilization, surreptitiously if possible, from "high' males: correspondingly, in the case of birds, "low' males may parasite by encouraging egg dumping in their nests by "high' females who have allowed copulation. It follows that nests of birds of low status should sometimes show evidence at times of both types of parasitism while nests of high status should show faithful monogamy. Showiness in monogamous species is more likely to be related to such extra-pair objectives than to pair-bonding for nesting. -from Author
Examined a wintering Parus atricapillus population in Connecticut, which has been studied for 26yr. There was strong evidence of lower survival rates in 1st-yr birds than in adults, but this could be the result of higher mortality rates, higher emigration rates, or a combination of the two. Survival rates of adult birds were not constant with age but decreased at a rate of approx 3.5%yr. As adult birds are very faithful to their wintering areas, almost all this decrease can be attributed to an increase in mortality with age.-from Authors
Survival from 1984 to 1985 was compared among known-aged California Gulls 4-23 yr old. Data supported a hypothesis of increasing reproductive effort with age. A flood during 1984 terminated breeding during the incubation phase of part of the colony, thus permitting an estimate of reproductive costs. Yearly survival of gulls whose nest flooded was 92% compared to 72% among gulls that carried out the reproductive cycle. Adult survival was inversely related to level of fledging success in 1984. Survival declined and fledging success increased with increasing age. However, gulls of differing ages within the same fledging success category had the same probability of survival. No evidence supported the hypothesis that fledging success increased with age because disproportionately larger numbers of individuals with @'good phenotypes@' survived to old age. Cross-sectional data showed that fledging success peaked at ages 16-19 and declined among gulls 20-23, suggesting senescence in extremely old gulls. However, longitudinal data indicated that fledging success did not decline among old gulls. The few gulls surviving to extreme old age did so by consistently exerting low reproductive effort and fledging few offspring.
(1) Continuous monitoring of a colony of marked kittiwakes has led to 34 years of data on the survival of individual birds, as well as on breeding success, mate fidelity and site tenacity. (2) Generalized linear modelling showed that the annual adult survival rate of the kittiwake varied according to sex, time-period, breeding experience and nest position. The effect of each factor was apparently independent of those of the other three. (3) The average annual survival rate of adult males was 78% and that of females 82%, after allowing for the effects of factors other than sex. Throughout the study, the survival odds for males were 0.8 times those for females. (4) First-time breeders survived as well as experienced birds which had been breeding for up to 12 years; beyond 12 years, the annual survival rate dropped by 11% on average. (5) Long-term changes in the annual adult survival rate of the kittiwake were not an artefact of the changing age structure of the colony through time. After removing the effect of age, the annual survival rate was highest during 1958-61, lowest during 1982-85; between these two periods, the mortality rate tripled. (6) Kittiwakes which settled in either the centre or the edge of the colony did so for life. Males and females that nested in the centre survived better than ones on the edge throughout the study (average of 81.2% versus 78.7% year-1). The difference probably reflected a segregation between intrinsically fit and less fit individuals: the two areas were equally safe to nest in, but centre birds had a higher breeding success and lifetime reproductive fitness than edge birds.
Age-specific mortality is measured to characterize the costs of reproduction in the beetle Callosobruchus maculatus, providing explicit details of the timing, duration, magnitude, and acceleration of mortality. We experimentally manipulated reproductive effort in four cohorts of 200 individually housed females by controlling exposure to males and to an artificial oviposition substrate. We demonstrate that (1) early reproduction produces long-term increases in age-specific mortality; (2) egg-laying effort affects the onset of age-specific mortality but not its shape or rate of change; and (3) mating with subsequent reproduction increases the rate of change in age-specific mortality relative to virgins. Accelerated senescence is defined demographically as an increase in the rate of change of age-specific mortality. Our results challenge the hypothesis that reproductive effort accelerates senescence but provides evidence that mating itself may have this effect.
Laying hens were placed on either a control diet or a carotenoid-supplemented diet. The subsequent concentrations of carotenoids in the yolks of the newly laid fertile eggs (μg carotenoid/g fresh yolk) were 13.3 and 41.1 on the control diet and high-carotenoid diet, respectively. For the day-old chicks derived from the high-carotenoid group, the carotenoid levels in the yolk sac membrane, liver, and plasma were approximately 3 times greater than in the control group; however, the other tissues were less responsive. The proportion of lutein (% wt/wt of total carotenoids) was far lower in the liver of the chick than in the yolk. However, in the non-hepatic tissues the proportion of lutein was generally higher than in the yolk. This suggests that discrimination between different carotenoids may occur in the embryo. For the high-carotenoid group, the peroxidative susceptibility of extracts of the yolk, yolk sac membrane, and liver was decreased compared with samples from the control group. Thus, carotenoids may provide antioxidant protection to the tissues.
A long-term study of marked individuals in a numerically stable Sparrowhawk breeding population enabled the reproductive and survival rates of females of different ages to be calculated. These estimates were then used to calculate reproductive value, the mean number of young produced by females of different ages during the rest of their lives. The data provided evidence, not only for improvement in survival and breeding success in the early years of life, but also for senescence, i.e., a deterioration in survival and breeding success later in life. Average annual survival increased from 0.49 in 1st-yr females to 0.66 in 4 yr olds, and declined to 0.28 in 9 yr olds (maximum life-span 10 yr). Average annual production of young increased from 0.3 in 1st-yr females (including nonbreeders) to 3.3 in 5 yr olds, and declined to 1.8 in 9 yr olds. Mean reproductive value increased from 3.1 in 1st-yr females (including nonbreeders) to 8.1 in 4 yr olds, and declined to 2.1 in 9 yr olds.
Birds live longer than mammals of comparable sizes, contrary to what their metabolic rates, plasma gulcose concentrations and body tempratures, all of which are higher than mammalian norms, would suggest. Although these factors should predispose them to accelerated tissue degeneration, this has been shown not to happen. In this paper the possible mechanism whereby birds limit the accelerated tissue damage that should be associated with the above characteristics are explored. Specifically, this review will focus on the relationship in chickens between the raised concentrations of plasma glucose and the lack of associated tissue complications. We propose that the role of uric acid in birds should be re-examined. Until now uric acid has been considered to be little more than an excretory by-product where its role as an antioxidant can be directly linked to the resistance of birds to glucose-mediated tissue damage. It is suggested that, compared with mammals, the lower rate of generation of reactive oxygen species in birds in association with their stronger antioxidant-defence system contributes to their longevity.
Here, I use published mortality data from 56 natural populations of mammals to examine evidence for senescence, an increase in the probability of mortality with age. Data on extent of senescence and life history characteristics are compared across taxa in an attempt to test theories for the evolution of senescence in natural populations. In accord with theoretical expectation, senescence is highest in short-lived species with short generation times. In contrast to theoretical expectation, however, senescent increases in mortality rate do not begin until well after age at maturity in most cases. I also present evidence in support of the hypothesis that senescence will be lower in large-brained taxa.
1. Senescence reflects age-dependent changes in residual reproductive value. Annual survival rates of the barn swallow Hirundo rustica L. increased from 1- to 2-year-old individuals, but decreased among 5 years old or older individuals. Estimates of age-dependent reproductive value showed a similar pattern.
2. Longitudinal data from two long-term population studies were used to test whether a number of different measures of performance (condition-dependent morphological traits, migratory performance, reproductive success, intensity of parasitism) changed among individuals when reaching old age.
3. The length of the outermost tail feathers (a secondary sexual character) decreased among old individuals, while two measures of individual developmental instability increased with age. Migratory performance decreased in old barn swallows as reflected by a delay in spring arrival at the breeding grounds. Reproductive performance measured as seasonal reproductive success decreased with age. The intensity of infestations with an haematophagous mite and a mallophagous ectoparasite increased among old barn swallows.
4. These results suggest that the condition-dependent secondary sexual character, developmental stability, and measures of migratory and reproductive performance deteriorated, and the frequency of parasitism increased among old individuals. Ageing was thus associated with a general deterioration of performance.
The aim of this study was to assess the differences in yolk lipid composition of pheasants and geese between birds maintained in captivity on commercial grain-based diets and their counterparts in the wild which are free to select their diets from the environment. The most striking difference was that the proportion of α-linolenic acid (18:3n-3) was far greater in all yolk lipid classes [triacylglycerol (TAG), phospholipid (PL), cholesteryl ester (CE)] of the wild birds than in the captive birds of both species. For example, in yolk TAG, the level (wt.% of total fatty acids) of 18:3n-3 was only 1.6% in eggs of captive pheasants compared with 27.9% in eggs of the wild birds. The proportions of 18:3n-3 in yolk TAG of housed, free-range and feral geese were 0.6, 6.6 and 19.3% respectively. It is suggested that these differences arise from the predominance of linoleic acid (18:2n-6) as the major polyunsaturate in the commercial grain-based feeds whereas geese and pheasants in the wild consume grasses and green shoots in which 18:3n-3 is the main fatty acid. The concentrations of vitamin E and carotenoids in the yolks of the free-range and feral geese were much greater than in those of the housed geese. Thus the developing embryos of pheasants and geese in the wild will have access to far higher levels of n-3 polyunsaturates and lipid-soluble antioxidants compared with embryos of the housed birds.
Theories of animal signalling emphasize the importance of costliness—to be effective, signals must be dependable; to be dependable, signals must carry costs—and carotenoid-based signals are a favoured example. The traditional view that carotenoids are costly because they are scarce still carries weight. However, biomedical research has led to alternative views on costliness, mainly related to beneficial, but also to detrimental, effects of carotenoids. Recent improvements in our understanding of carotenoids suggest that the relative importance of these mechanisms will soon be determined, leading to a fresh outlook on cost-based signalling.
Describes how organisms behave and live in relation to their environment and evolutionary history, bearing in mind the different resources that are required, and the nature of the interactions between these resources. The balance between birth rates and death rates, which indicates abundance, is shown to have profound effects on the behaviour of populations. Dispersal of organisms is linked with escape from unfavourable environments and the colonisation and exploitation of new environments. In looking at interactions between organisms, the nature and consequences of intra- and interspecific competition are explored. The nature of predation and grazing, behaviour of consumers and consumed, and implications of predation/grazing for population dynamics are also discussed. Decomposition and detritivore trophic linkages are reviewed, as are parasitism and disease. The evolution of mutualistic relationships is noted. Surveys of the range of life history strategies exhibited by living organisms, and of the range of patterns of abundance, are used to provide overviews of the organismic and the population levels in the ecological hierarchy. The final section considers interactions at the community level, looking at how community patterns change through space and time, examining the flux of energy and matter through communities, and indicating the influence of competition, predation and disturbance on community structure. Aspects of island biogeography theory are also discussed. The final chapters examine community stability and structure, and patterns of species diversity. -P.J.Jarvis
Featuring extensive references, updated for this paperback edition, Longevity, Senescence, and the Genome constitutes a landmark contribution to biomedicine and the evolutionary biology of aging. To enhance gerontology's focus on human age-related dysfunctions, Caleb E. Finch provides a comparative review of all the phyla of organisms, broadening gerontology to intersect with behavioral, developmental, evolutionary, and molecular biology. By comparing species that have different developmental and life spans, Finch proposes an original typology of senescence from rapid to gradual to negligible, and he provides the first multiphyletic calculations of mortality rate constants.
"This book is well worth buying for its detailed summaries of the 25 studies, many of which are classic long-term projects, and for its insights into the factors determining reproductive success."âWilliam J. Sutherland, TREE "A must read for anyone interested in evolution, mating/social systems, and population ecology."âJohn L. Koprowski, IJournal of Insect Behavior
This study examined age-related changes in six measures of reproductive success for captive Falco peregrinus. Mean nestling survivorship increased throughout the lifespan of the female while all other measures of reproduction peaked at about seven years of age and decreased thereafter. Birds with prior breeding experience had higher productivity than inexperienced birds of the same age. Productivity increased with increasing experience of the pair. Productivity dropped by an average of 53% when females experienced a change of mate, and then subsequently increased over a period of several years. Lifetime reproduction was not correlated with longevity because birds with higher maximal egg production have shorter breeding lifespans. -from Author
When strong positive heritability of fitness arises due to host-parasite coevolution, consequent sosigonic mate preference undermines monogamy through tendencies to extra-pair copulation. “Low” females bonded to “low” males try to parasitise their partnership by obtaining fertilization, surreptitiously if possible, from “high” males: correspondingly, in the case of birds, “Low” males may parasite by encouraging egg dumping in their nests by “high” females who have allowed copulation. It follows that nests of birds of low status should sometimes show evidence at times of both types of parasitism while nests of high status should show faithful monogamy.
Rather differently from the argument in Hamilton and Zuk (1982), showiness in monogamous species is more likely to be related to such extra-pair objectives than to pair—bonding for nesting.
Venereal disease makes males cautious about copulating with any female. Although prevented by true monogamy, when monogamy is partial, venereal disease may become the incentive for increasing female sexual advertisement. In extreme cases it may combine with other ecological factors to initiate sex role reversal, in which the female becomes the non-parenting sex of the species.
As regards source of the heritability that backs the sosigonic selection assumed in such speculations, reasons are given for preferring a coevolutionary cycling of ancient, preserved, parasite-defense alleles to the alternatives of an abundant stream of good new defense mutations, or a process of elimination of purely deleterious mutations.
Evolutionary considerations predict that rate of aging should vary in direct relation to the mortality rate of presenescent young adults (extrinsic mortality rate) independently of differences in physiology, such as rate of metabolism. This prediction emerges from theory irrespective of the particular genetic mechanisms responsible for variation in aging. Yet this critical relationship has not been confirmed in comparative studies of natural populations. In the present analysis, rate of aging is estimated by the rate of increase in mortality rate (mx) with age (x). Comparisons between natural and captive populations of birds suggest that the Weibull model (mx = m0 + alphaxbeta) provides a better description of aging than the Gompertz model (mx = m0esigmax). Rate of aging is quantified by the parameter omega (dimension: 1/time), which is calculated from the Weibull parameters alpha and beta (omega = alpha1/(beta+1)). In this analysis, rate of aging in birds and mammals is directly related to extrinsic mortality (estimated by the initial mortality rate, m0) independently of taxonomic group and of variation in body size and, by implication, metabolic rate. When time is expressed in years, rate of senescence is related to initial mortality rate by omega = 0.294m0(0.367). This result implies that natural selection in response to variation among taxa in m0 has resulted in the evolutionary modification of factors that influence the rate of aging in natural populations. The potential strength of selection on factors that could further reduce rate of aging is indicated by the proportion of deaths due to aging-related causes. Although species with low initial mortality rates also exhibit reduced rates of increase in mortality rate with age (i.e., delayed senescence), the relatively high proportion of aging-related deaths in such species suggests that further evolutionary responses leading to long life are severely constrained. This argues against mutation accumulation and antagonistic pleiotropy as genetic mechanisms underlying senescence and suggests, instead, that rate of aging represents a balance between wear and tear, on the one hand, and genetically controlled mechanisms of prevention and repair, on the other. Evidently, remedies for extreme physiological deterioration in old age either are not within the range of genetic variation or are too costly to be favored by selection.
Most modern theories of aging have centered around the notion that age-related deterioration is primarily due to structural
and functional modifications of cellular constituents. Among them are three currently popular hypotheses — the free radical,
Glycation, and Maillard Theories of Aging. The first proposes that age-related effects are due to free radical reactions that
damage cellular constituents, while the latter propose damage induced by nonenzymatic gly cation and other maillard reactions
and the consequent modification of macromolecules as the primary cause of aging. Although these hypotheses were formulated
independently, recent studies suggest that free radicals, glycation, and maillard reactions may in fact represent partially
interactive elements of a single, more complex biochemical pathway. We therefore propose the free Radical-Glycation/maillard
reaction theory of aging: that age-related deterioration is produced by the sum of the damage induced by free radicals, by
glycation, by Maillard reactions, and by their interactions
In order to prevent or escape the ongoing damage to proteins and DNA resulting from amino-carbonyl reactions, the organism has to have powerful defense mechanisms. If the Maillard reaction played a role in determining longevity among mammalian species, one would expect protective mechanisms to be more developed in long- versus short-lived species. This article summarizes current knowledge in this field, and discusses the concept of anti-Maillard mechanisms as a basis for the genetic regulation of molecular damage by reducing sugars in aging and diabetes.
Birds are widely distributed, highly diversified, and exhibit behavior and social organizations equal in complexity to mammals,
yet they are generally more conspicuous and approachable in natural environments. These attributes make birds excellent subjects
in many areas of biological research. The topics in which studies on birds have figured prominently include the mechanisms
of species formation, the regulation of the distribution and abundance of animals, the effects of the environment on behavior
and physiology, the biological and evolutionary significance of variations in social organizations, the encoding of information
in animal communication, the sensory basis for migration and navigation, the effects of hormones on nerve cells and behavior,
the ontogeny of brain and behavior, and the structure and function of the vertebrate brain. The outstanding record of avian
research suggests that birds will continue to provide important models for developing and testing new ideas in various fields
of biology.
The loss of biologic function by the nonenzymatic reaction of glucose with proteins and nucleic acids offers a new way to explain the chemical basis of aging. This hypothesis is attractive because it could explain both the age-related changes noted with extracellular proteins as well as cells. The amount of accumulated advanced glycosylation endproducts (AGE) present on biopolymers at any time is a function of the rate of formation and removal. Increasing the amount of glucose or reducing sugar promotes by the law of mass action an accelerated rate of AGE formation. Many of the age-associated disorders and diseases (eg, cataracts, atherosclerosis) occur at a younger age in diabetics than normal people. In fact, the complications of diabetic patients are frequently put forth as a paradigm for aging. Because most patients with diabetes are hyperglycemic, there is an increased amount of glucose modified proteins with altered biologic activity. The study of this metabolic disorder should give new insight to the general aging mechanism. Previously, we had believed that the removal of glucose-modified proteins was equivalent to the turnover of that particular protein in the body. However, the recent finding of a senescent-protein removal system in the macrophage prompts one to question whether other removal systems might also be present in cells for removing AGE-proteins or AGE-DNA. Although substantially more evidence is necessary to strengthen the hypothesis presented herein, it presents a model around which to consider clinical correlates and design future experiments. These future experiments will hopefully give new insight into the possible role of glucose as one of the important mediators of aging.
Aminophenylboronic acid affinity chromatography was used to measure glycosylated hemoglobin and glycosylated albumin levels in a variety of species. The highest glycosylated hemoglobin levels were found in man, the lowest in the chicken and the pig. The highest glycosylated albumin levels were found in avian species, the lowest in the mouse and the rat. A simple kinetic model was used to analyze the rates of formation of glycosylated hemoglobin and albumin in the various species. Rates of glycosylated albumin formation were very similar across the species while rates of glycosylated hemoglobin formation were quite different, presumably reflecting wide differences in erythrocyte permeability to glucose among the species.
Evolutionary pressure induced by the release of O2 into the environment has necessitated the development of a group of mechanisms to deal with the toxic free radical byproducts of oxidative metabolism. The complete reduction of O2 to H2O2 involves the addition of four electrons which can occur univalently resulting in a series of toxic intermediates or quadrivalently by the mitochondrial cytochrome oxidase system, which avoids these reactive intermediates. Free radical mechanisms have been associated with a large number of disease states including inflammation, irradiation-induced injury and ischemia. The site of free radical generation, that is whether the generation of radical species is predominantly extracellular or intracellular, may determine to a degree, the types of macromolecular and cellular damage which result. A classification of diseases in which radical generating processes may play a role is presented in the hope that it may aid in the understanding and treatment of these diseases.
A polyclonal antibody specific for the Amadori compound, a product of an early stage of the Maillard reaction, was raised in rabbits by immunization with hexitol-lysine (1-glucitol-lysine or 1-mannitol-lysine) coupled with various carrier proteins. The affinity purified antibody has a high titre and preferentially recognizes the glucose adduct, in the presence of sodium borohydride, as judged on enzyme-linked immunosorbent assay as well as immunoblot analysis. The glycated proteins (Amadori products) in various tissues of normal and streptozotocin-induced diabetic rats were examined by immunoblot analysis. In diabetic conditions, kidney, liver, lens, brain and lung proteins are more susceptible to glycation than other tissue proteins. Heart, spleen, adrenal gland and muscle proteins exhibit similar extents of glycation in both normal and diabetic conditions. This is the first demonstration of a specific antibody against the Amadori compound being raised with a synthetic compound, and of the tissue distribution of glycated proteins in normal and diabetic conditions. The antibody was very useful for in vitro and in vivo experiments on the Maillard reaction.
Advanced glycation end products (AGEs) and glycoxidation products are formed during Maillard or browning reactions between sugars and proteins and are implicated in the pathophysiology of aging and the complications of diabetes. To determine the structure of AGEs, antibodies were prepared to protein browned by incubation with glucose and used in ELISA assays to measure AGEs formed in model reactions between bovine serum albumin (BSA) or N alpha-acetyllysine and glucose, fructose, or glyoxal. AGEs were formed from glucose and fructose only under oxidative conditions, but from glyoxal under both oxidative and antioxidative conditions. Gel permeation chromatographic analysis indicated that a similar AGE was formed in reactions of N alpha-acetyllysine with glucose, fructose, and glyoxal and that this AGE co-eluted with authentic N alpha-acetyl-N epsilon-(carboxymethyl)lysine. Amino acid analysis of AGE proteins revealed a significant content of N epsilon-(carboxymethyl)lysine (CML). In ELISA assays using polyclonal antibodies against AGE proteins, CML-BSA (approximately 25 mol of CML/mol of BSA), prepared by chemical modification of BSA, was a potent inhibitor of the recognition of AGE proteins and of AGEs in human lens proteins. We conclude that AGEs are largely glycoxidation products and that CML is a major AGE recognized in tissue proteins by polyclonal antibodies to AGE proteins.
Bird species are dramatically longer-lived than similar-sized mammals, in spite of two traits--high metabolic rate and elevated blood glucose--which some modern theories of aging suggest should be associated with accelerated senescence. As a consequence of their longevity, birds may possess specialized protective mechanisms against free radical and Maillard reaction damage, and may offer insight into medical interventions for retarding aging. In this review we have highlighted a number of bird species which are commercially available, easily maintained, and more thoroughly characterized with respect to basic physiology than many biogerontologists realize. There seem to us to be few intrinsic barriers to the development of several avian "mice"--extensively characterized species exhibiting exceptionally long life and retarded aging--and for these to become readily accessible as a laboratory resource for the gerontological research community.
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.
Attack by reactive oxygen intermediates, common to many kinds of cell/tissue injury, has been implicated in the development of diabetic and other vascular diseases. Such oxygen-free radicals can be generated by advanced glycation end products (AGEs), which are nonenzymatically glycated and oxidized proteins. Since cellular interactions of AGEs are mediated by specific cellular binding proteins, receptor for AGE (RAGE) and the lactoferrin-like polypeptide (LF-L), we tested the hypothesis that AGE ligands tethered to the complex of RAGE and LF-L could induce oxidant stress. AGE albumin or AGEs immunoisolated from diabetic plasma resulted in induction of endothelial cell (EC) oxidant stress, including the generation of thiobarbituric acid reactive substances (TBARS) and resulted in the activation of NF-kappa B, each of which was blocked by antibodies to AGE receptor polypeptides and by antioxidants. Infusion of AGE albumin into normal animals led to the appearance of malondialdehyde determinants in the vessel wall and increased TBARS in the tissues, activation of NF-kappa B, and induction of heme oxygenase mRNA. AGE-induced oxidant stress was inhibited by pretreatment of animals with either antibodies to the AGE receptor/binding proteins or antioxidants. These data indicate that interaction of AGEs with cellular targets, such as ECs, leads to oxidant stress resulting in changes in gene expression and other cellular properties, potentially contributing to the development of vascular lesions. Further studies will be required to dissect whether oxidant stress occurs on the cell surface or at an intracellular locus.