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Adult-onset, short-term dietary restriction reduces cell senescence in mice.

Wang C, Maddick M, Miwa S, Jurk D, Czapiewski R, Saretzki G, Langie SA, Godschalk RW, Cameron K, von Zglinicki T - Aging (Albany NY) (2010)

Bottom Line: This reduction was associated with improved telomere maintenance without increased telomerase activity.We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level.The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrated Systems Biology of Ageing and Nutrition, Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK.

ABSTRACT
Dietary restriction (DR) extends the lifespan of a wide variety of species and reduces the incidence of major age-related diseases. Cell senescence has been proposed as one causal mechanism for tissue and organism ageing. We show for the first time that adult-onset, short-term DR reduced frequencies of senescent cells in the small intestinal epithelium and liver of mice, which are tissues known to accumulate increased numbers of senescent cells with advancing age. This reduction was associated with improved telomere maintenance without increased telomerase activity. We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level. The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.

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Related in: MedlinePlus

DR does not change oxidative damage markers measured in whole liver homogenates.(A) 8-oxodG levels in liver homogenates from AL and DR mice measured by HPLC with electrochemical detection. n=9 animals/group. (B) Nitrotyrosine levels in liver homogenates from AL and DR mice measured by ELISA; n=6 animals/ group. (C) Steady state hydrogen peroxide release from liver homogenates from AL and DR mice measured by Amplex Red fluorimetry; n=12 animals/ group. All data are mean ±S.E.M.; n.s.: not significant (T-test).
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Figure 5: DR does not change oxidative damage markers measured in whole liver homogenates.(A) 8-oxodG levels in liver homogenates from AL and DR mice measured by HPLC with electrochemical detection. n=9 animals/group. (B) Nitrotyrosine levels in liver homogenates from AL and DR mice measured by ELISA; n=6 animals/ group. (C) Steady state hydrogen peroxide release from liver homogenates from AL and DR mice measured by Amplex Red fluorimetry; n=12 animals/ group. All data are mean ±S.E.M.; n.s.: not significant (T-test).

Mentions: 8-oxodG (a marker for oxidative DNA damage), nitrotyrosine content (a marker for oxidative protein damage) and H2O2 release rate from tissue homogenate are indicative of steady-state levels of oxidative stress/oxidative damage. These markers were measured in whole liver homogenates. None of them were significantly different between AL and DR mice (Figure 5). Similarly, DR did not change 8-oxodG levels in homogenates of the intestinal mucosa (data not shown).


Adult-onset, short-term dietary restriction reduces cell senescence in mice.

Wang C, Maddick M, Miwa S, Jurk D, Czapiewski R, Saretzki G, Langie SA, Godschalk RW, Cameron K, von Zglinicki T - Aging (Albany NY) (2010)

DR does not change oxidative damage markers measured in whole liver homogenates.(A) 8-oxodG levels in liver homogenates from AL and DR mice measured by HPLC with electrochemical detection. n=9 animals/group. (B) Nitrotyrosine levels in liver homogenates from AL and DR mice measured by ELISA; n=6 animals/ group. (C) Steady state hydrogen peroxide release from liver homogenates from AL and DR mice measured by Amplex Red fluorimetry; n=12 animals/ group. All data are mean ±S.E.M.; n.s.: not significant (T-test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2984605&req=5

Figure 5: DR does not change oxidative damage markers measured in whole liver homogenates.(A) 8-oxodG levels in liver homogenates from AL and DR mice measured by HPLC with electrochemical detection. n=9 animals/group. (B) Nitrotyrosine levels in liver homogenates from AL and DR mice measured by ELISA; n=6 animals/ group. (C) Steady state hydrogen peroxide release from liver homogenates from AL and DR mice measured by Amplex Red fluorimetry; n=12 animals/ group. All data are mean ±S.E.M.; n.s.: not significant (T-test).
Mentions: 8-oxodG (a marker for oxidative DNA damage), nitrotyrosine content (a marker for oxidative protein damage) and H2O2 release rate from tissue homogenate are indicative of steady-state levels of oxidative stress/oxidative damage. These markers were measured in whole liver homogenates. None of them were significantly different between AL and DR mice (Figure 5). Similarly, DR did not change 8-oxodG levels in homogenates of the intestinal mucosa (data not shown).

Bottom Line: This reduction was associated with improved telomere maintenance without increased telomerase activity.We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level.The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.

View Article: PubMed Central - PubMed

Affiliation: Centre for Integrated Systems Biology of Ageing and Nutrition, Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK.

ABSTRACT
Dietary restriction (DR) extends the lifespan of a wide variety of species and reduces the incidence of major age-related diseases. Cell senescence has been proposed as one causal mechanism for tissue and organism ageing. We show for the first time that adult-onset, short-term DR reduced frequencies of senescent cells in the small intestinal epithelium and liver of mice, which are tissues known to accumulate increased numbers of senescent cells with advancing age. This reduction was associated with improved telomere maintenance without increased telomerase activity. We also found a decrease in cumulative oxidative stress markers in the same compartments despite absence of significant changes in steady-state oxidative stress markers at the whole tissue level. The data suggest the possibility that reduction of cell senescence may be a primary consequence of DR which in turn may explain known effects of DR such as improved mitochondrial function and reduced production of reactive oxygen species.

Show MeSH
Related in: MedlinePlus