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PubMed1993

Biochemical correlates of longevity in two closely related rodent species.

The objective of this study was to explore the basis of variations in the life span and metabolic potential, i.e., total amount of energy consumed during life, between different species, in context of the free radical hypothesis of aging. A comparison was made between the house mouse (Mus musculus) and the white-footed mouse (Peromyscus leucopus): the latter has > 2-fold greater life span and metabolic potential than the former. Longer life span and higher metabolic potential of Peromyscus were associated with low rates of mitochondrial O2.- and H2O2 generation, higher activities of catalase and glutathione peroxidase and low levels of protein oxidative damage as well as low susceptibility to oxidative damage in response to experimental oxidative stress. Results support the role of oxidative stress in aging.

Aging↗
PubMed1994

DNA repair and the evolution of longevity: a critical analysis.

Comparative gerontologists argue that variation among species in DNA repair rates may explain differences in maximum lifespan, and support this claim with the observation that DNA repair rates and lifespan correlate positively among mammals. However, these findings may be confounded by both size and phylogeny. Repair rates and lifespan may be positively correlated because both are positively correlated with body size. In addition, previous comparative studies have not controlled for the potentially confounding effects of phylogeny. In this study, I elucidate why we might expect larger species to have higher DNA repair rates, independent of differences in lifespan, and use existing data to test whether the relationship between DNA repair rates and lifespan holds up after controlling for the potentially confounding effects of size and phylogeny. Reanalysis of the existing data suggests that there is little comparative evidence in favour of the hypothesis relating DNA repair rates and lifespan.

Animals↗
PubMed2001

A stochastic model for CD8(+)T cell dynamics in human immunosenescence: implications for survival and longevity.

We propose here a stochastic model for the CD 8(+)T lymphocyte dynamics on the long time-scale of the human lifespan. Our purpose has been to test the hypothesis, recently proposed on the basis of our experimental data (Fagnoni et al., 2000), that the depletion of virgin CD8(+)T lymphocytes can be considered a reliable biomarker related to the risk of death. This hypothesis is embedded in a more general theory of immunosenescence according to which the accumulation of antigen experienced (AE) T cells and the concomitant exhaustion of antigen non-experienced (ANE) T cells with age, mostly due to the chronic lifelong exposure to antigens, is a major characteristic of the remodeling of the human immune system with age. In our model we considered a deterministic balance of ANE and AE T cell concentrations plus a stochastic forcing, which describes the chronic antigenic stress fluctuations, assuming a mean genetically determined capability of individuals to respond to antigens. The major results of our model is the validation of the above-mentioned hypothesis, since the model is capable of fitting the experimental data concerning the changes of ANE T cell concentration over age, and at the same time to reproduce survival curves similar to the demographic ones. Furthermore, the stochastic process results in being responsible for the peculiar shape of the survival curves.

Aging↗