Urinary excretion of dna repair products correlates with metabolic rates as well as with maximum life spans of different mammalian species

Foksiński, Marek; Różalski, Rafał; Guz, Jolanta; Ruszkowska, Barbara; Sztukowska, Paulina; Piwowarski, Maciej; Klungland, Arne; Oliński, Ryszard

doi:10.1016/j.freeradbiomed.2004.07.014

Cited by 96 publications

(72 citation statements)

References 37 publications

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“…5b; data re-plotted from Barja and Herrero 2000); (4) urinary excretion of multiple DNA repair end products is significantly greater in smaller species, and inversely correlated with body mass (Fig. 5c; data re-plotted from Foksinski et al 2004). These disparate results are well reconciled by the observation here that some BER activities are also elevated in brain and liver of smaller species and correlate negatively with body mass.…”

Section: Discussionmentioning

confidence: 53%

“…Taken together, these multiple two-species comparisons do not consistently support the hypothesis that BER activities are elevated in longer-lived species. Species' body mass is negatively correlated with a mitochondrial ROS production (heart data from Ku et al (1993) re-plotted against body mass); b urinary 8-oxodG excretion (data from Foksinski et al (2004) re-plotted against body mass); and c nuclear DNA 8-oxodG levels (heart data from Barja and Herrero (2000) re-plotted against body mass)…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, shorter-lived mammalian species, which tend also to be smaller, do not show elevated levels of oxidative damage in nuclear DNA in all tissues (Barja and Herrero 2000), despite apparently higher rates of respiratory ROS production owing to greater mitochondrial abundance (e.g., Porter and Brand 1995) and enhanced ROS production per mitochondrion (e.g., Lambert et al 2007). An important observation is that these smaller and shorter-lived species also excrete higher levels of stable DNA repair end products in their urine (Foksinski et al 2004), which presumably indicates higher rates of repair. Taken together, these observations are consistent with the hypothesis that smaller, shorter-lived species with higher mass-specific metabolic rates sustain more DNA oxidative damage in their highly oxidative tissues but also repair it rapidly, thus leading to greater rates of excretion of DNA repair end products.…”

Section: Introductionmentioning

confidence: 99%

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Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

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Stuart

2011

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Accumulation of DNA lesions compromises replication and transcription and is thus toxic to cells. DNA repair deficiencies are generally associated with cellular replicative senescence and premature aging syndromes, suggesting that efficient DNA repair is required for normal longevity. It follows that the evolution of increasing lifespan amongst animal species should be associated with enhanced DNA repair capacities. Although UV damage repair has been shown to correlate positively with mammalian species lifespan, we lack similar insight into many other DNA repair pathways, including base excision repair (BER). DNA is continuously exposed to reactive oxygen species produced during aerobic metabolism, resulting in the occurrence of oxidative damage within DNA. Shortpatch BER plays an important role in repairing the resultant oxidative lesions. We therefore tested whether an enhancement of BER enzyme activities has occurred concomitantly with the evolution of increased maximum lifespan (MLSP). We collected brain and liver tissue from 15 vertebrate endotherm species ranging in MLSP over an order of magnitude. We measured apurinic/ apyrimidinic (AP) endonuclease activity, as well as the rates of nucleotide incorporation into an oligonucleotide containing a single nucleotide gap (catalyzed by BER polymerase β) and subsequent ligation of the oligonucleotide. None of these activities correlated positively with species MLSP. Rather, nucleotide incorporation and oligonucleotide ligation activities appeared to be primarily (and negatively) correlated with species body mass.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

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Stuart

2011

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“…Colon cancer originates from the epithelial cells that line the bowel. These cells divide rapidly and have a high metabolic rate [131]. Since the intestinal mucosa is constantly confronting with diet and bacterial-derived oxidants and carcinogens, an unrestrained production of free radicals, redox imbalance, and DNA damage occurs, finally leads to an altered intestinal metabolic homeostasis with cancer as an endpoint [133].…”

Section: Colorectal Cancermentioning

confidence: 99%

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases

2014

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Free radicals and other oxidants have gained importance in the field of biology due to their central role in various physiological conditions as well as their implication in a diverse range of diseases. The free radicals, both the reactive oxygen species (ROS) and reactive nitrogen species (RNS), are derived from both endogenous sources (mitochondria, peroxisomes, endoplasmic reticulum, phagocytic cells etc.) and exogenous sources (pollution, alcohol, tobacco smoke, heavy metals, transition metals,

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“…For example, mammals that live longer have lower urinary excretion rates of DNA excision-repair products (8-oxoGua and 8-oxodG) (Foksinski et al 2004), lower oxidative damage to mitochondria (8-oxodG in mitochondrial DNA) (Barja and Herrero 2000;Barja 2002), lower levels of fatty acid desaturation in heart phospholipids, and lower levels of dehydroepiandrosterone (DHEA) in heart phospholipids (Pamplona et al 1999). Moreover, since Rubner's time, the database of species for which both maximum lifespan and resting metabolism are available has increased enormously, and the fundamental observation that the product of these traits is independent of body size has, until recently, been repeatedly supported (Calder 1984;Prinzinger 2005).…”

Section: Introductionmentioning

confidence: 99%

Energetics and longevity in birds

Furness

Speakman

2008

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The links between energy expenditure and ageing are different at different levels of enquiry. When studies have examined the relationships between different species within a given class the association is generally negative-animals with greater metabolism per gram of tissue live shorter lives. Within species, or between classes (e.g. between birds and mammals) the association is the opposite-animals with higher metabolic rates live longer. We have previously shown in mammals that the negative association between lifespan and metabolic rate is in fact an artefact of using resting rather than daily energy expenditure, and of failing to adequately take into account the confounding effects of body size and the lack of phylogenetic independence of species data. When these factors are accounted for, across species of mammals, the ones with higher metabolism also have the largest lifetime expenditures of energy-consistent with the inter-class and intra-specific data. A previous analysis in birds did not yield the same pattern, but this may have been due to a lack of sufficient power in the analysis. Here we present an analysis of a much enlarged data set (>300 species) for metabolic and longevity traits in birds. These data show very similar patterns to those in mammals. Larger individuals have longer lives and lower per-gram resting and daily energy expenditures, hence there is a strong negative relationship between longevity and mass-specific metabolism. This relationship disappears when the confounding effects of body mass and phylogeny are accounted for. Across species of birds, lifetime expenditure of energy per gram of tissue based on both daily and resting energy expenditure is positively related to metabolic intensity, mirroring these statistical relationships in mammals and synergising with the positive associations of metabolism with lifespan within species and between vertebrate classes.

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Urinary excretion of dna repair products correlates with metabolic rates as well as with maximum life spans of different mammalian species

Cited by 96 publications

References 37 publications

Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

Activities of DNA base excision repair enzymes in liver and brain correlate with body mass, but not lifespan

Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases

Energetics and longevity in birds

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