These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Age-related oxidative inactivation of Na+, K+-ATPase in rat brain crude synaptosomes.
    Author: Chakraborty H, Sen P, Sur A, Chatterjee U, Chakrabarti S.
    Journal: Exp Gerontol; 2003 Jun; 38(6):705-10. PubMed ID: 12814807.
    Abstract:
    The study was undertaken to examine the status of Na(+), K(+)-ATPase in aged rat brain and to verify if any alteration of this enzyme in aged brain could be related to an oxidative damage. The crude synaptosomes from rat brain were exposed in vitro to an oxidative stress in the form of a combination of Fe(2+) (100 microM) and ascorbate (2 mM) for up to 2 h when increased lipid peroxidation (nearly four-fold), extensive protein carbonyl formation and a marked decrease of Na(+), K(+)-ATPase activity (approximately 88%) were observed. All these changes were prevented by the presence of a chain-breaking anti-oxidant, butylated hydroxytoluene (0.2 mM), in the incubation mixture. When the same crude synaptosomal membranes from the young (4-6 months) and aged (18-22 months) rat brains were analysed, a significant reduction of Na(+), K(+)-ATPase activity (nearly 48%) along with significantly elevated levels of lipid peroxidation products and protein carbonyls could be detected in the aged animals in comparison to young ones. The latter data in combination with the results of in vitro experiments imply that the age-related decline of rat brain Na(+), K(+)-ATPase activity is presumably the consequence of an enhanced oxidative damage in aging brain
    [Abstract] [Full Text] [Related] [New Search]