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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
CHANGES IN XANTHINE OXIDASE ACTIVITY AND LIPID PEROXIDATION LEVELS IN PREMATURELY AGING MICE
Abstract number: P54
Vida1 C, De Castro1 NM, Corpas1 I, De la Fuente1 M, Gonzalez1 E
1Department of Animal Physiology. Faculty of Biology. Complutense University of Madrid. 28040 Madrid, Spain. [email protected]
Aim:
Xanthine oxidase is a key enzyme of purine catabolism that catalyzes the oxidation of a wide range of substrates and therefore generates reactive oxygen species. The aging process has as its base a chronic oxidative stress, with an excessive production of reactive oxygen species which subsequently leads to oxidative damage of molecules (lipids, proteins and DNA). In this study, we have investigated the xanthine oxidase activity and lipid peroxidation in different organs of prematurely aging mice.
Methods:
Adult female Balc/C mice were classified as Non Prematurely Aging Mice (NPAM) or Prematurely Aging Mice (PAM) according to their performance in a T-maze behavioural test. This test took place once a week during four consecutive weeks. Afterwards, the mice were sacrificed and liver, kidney and spleen were obtained in order to determine xanthine oxidase activity and lipid peroxidation. Xanthine oxidase activity of tissue samples was determined using the "Amplex Red Xathine/XO Assay" kit. Lipid peroxidation was determined by the thiobarbituric acid-reactive substances (TBARS) assay.
Results:
Xanthine oxidase activity was significantly increased in liver and kidney of PAM mice, however no significant difference was observed in spleen. TBARs production was significantly higher in the liver in PAM-mice compared to NPAM. No significant differences were detected in kidney and spleen.
Conclussion:
In summary, the results show that the oxidation state, measured by xanthine oxidase activity and TBARs levels, is, in general, higher in prematurely aging mice an may be partially responsible for their premature mortality.
Financial support: MEC (BFU2005-06777); MICINN (BFU2008-04336) and Group of Research UCM (910379ENEROINN) grants. RETICEF (RD06/0013/0003).
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P54