• Institut für Biomedizinische Alternsforschung

IBA Publikation

Bild






IBA Publikation


epub.oeaw – Institutionelles Repositorium der Österreichischen Akademie der Wissenschaften
epub.oeaw – Institutional Repository of the Austrian Academy of Sciences
A-1011 Wien, Dr. Ignaz Seipel-Platz 2
Tel. +43-1-515 81/DW 3420, Fax +43-1-515 81/DW 3400
http://epub.oeaw.ac.at, e-mail: epub@oeaw.ac.at

Bestellung/Order


Bild






IBA Publikation
IBA Publikation







Send or fax to your local bookseller or to:

Verlag der Österreichischen Akademie der Wissenschaften
Austrian Academy of Sciences Press
A-1011 Wien, Dr. Ignaz Seipel-Platz 2,
Tel. +43-1-515 81/DW 3420, Fax +43-1-515 81/DW 3400
https://verlag.oeaw.ac.at, e-mail: bestellung.verlag@oeaw.ac.at
UID-Nr.: ATU 16251605, FN 71839x Handelsgericht Wien, DVR: 0096385

Bitte senden Sie mir
Please send me
 
Exemplar(e) der genannten Publikation
copy(ies) of the publication overleaf


NAME


ADRESSE / ADDRESS


ORT / CITY


LAND / COUNTRY


ZAHLUNGSMETHODE / METHOD OF PAYMENT
    Visa     Euro / Master     American Express


NUMMER

Ablaufdatum / Expiry date:  

    I will send a cheque           Vorausrechnung / Send me a proforma invoice
 
DATUM, UNTERSCHRIFT / DATE, SIGNATURE

BANK AUSTRIA CREDITANSTALT, WIEN (IBAN AT04 1100 0006 2280 0100, BIC BKAUATWW), DEUTSCHE BANK MÜNCHEN (IBAN DE16 7007 0024 0238 8270 00, BIC DEUTDEDBMUC)
Bild






IBA Publikation

Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice

    L.M. Guachalla, Z. Ju, R. Koziel, G. von Figura, Z. Song, M. Fusser, B. Epe, P. Jansen-Dürr, K. L. Rudolph

IBA Publikation, pp. 303-315, 2009/11/05


Object
X
BibTEX-Export:

X
EndNote/Zotero-Export:

X
RIS-Export:

X 
Researchgate-Export (COinS)

Permanent QR-Code

Abstract

Abstract: Telomere shortening represents a causal factor of cellular senescence. At the same time, several lines of evidence indicate a pivotal role of oxidative DNA damage for the aging process in vivo. A causal connection between the two observations was suggested by experiments showing accelerated telomere shorting under conditions of oxidative stress in cultured cells, but has never been studied in vivo. We therefore have analysed whether an increase in mitochondrial derived oxidative stress in response to heterozygous deletion of superoxide dismutase (Sod2+/-) would exacerbate aging phenotypes in telomere dysfunctional (mTerc-/-) mice. Heterozygous deletion of Sod2 resulted in reduced SOD2 protein levels and increased oxidative stress in aging telomere dysfunctional mice, but this did not lead to an increase in basal levels of oxidative nuclear DNA damage, an accumulation of nuclear DNA breaks, or an increased rate of telomere shortening in the mice. Moreover, heterozygous deletion of Sod2 did not accelerate the depletion of stem cells and the impairment in organ maintenance in aging mTerc-/- mice. In agreement with these observations, Sod2 haploinsufficiency did not lead to a further reduction in lifespan of mTerc-/- mice. Together, these results indicate that a decrease in SOD2-dependent antioxidant defence does not exacerbate aging in the context of telomere dysfunction.