By Topic

Stress Response to Hypoxia in Wistar Rat: LA, MDA, SOD and Na+-K+-ATPase

Sign In

Cookies must be enabled to login.After enabling cookies , please use refresh or reload or ctrl+f5 on the browser for the login options.

Formats Non-Member Member
$33 $13
Learn how you can qualify for the best price for this item!
Become an IEEE Member or Subscribe to
IEEE Xplore for exclusive pricing!
close button

puzzle piece

IEEE membership options for an individual and IEEE Xplore subscriptions for an organization offer the most affordable access to essential journal articles, conference papers, standards, eBooks, and eLearning courses.

Learn more about:

IEEE membership

IEEE Xplore subscriptions

6 Author(s)
Dingyu Hu ; Sch. of Life Sci. & Technol., Beijing Inst. of Technol., Beijing, China ; Qin Li ; Bo Li ; Rongji Dai
more authors

To study the time course of oxidative damage and the molecular and cellular mechanisms underlying hypoxia-induced brain damage, some stress responses to hypoxia in rat brain, such as lactic acid(LA) and malondialdehyde (MDA) expression, superoxide dismutase (SOD) and Na+-K+-ATPase activity etc, were analysed. The role of those factors in oxidative stress was discussed too. Results showed that the SOD activity reduced obviously at 15% O2 and the level of MDA raised obviously at 12% O2, the level of lactic acid increased obviously and the Na+-K+-ATPase activity decreased obviously at 10% O2 respectively. Obviously this gave an inkling that the loss of ion homeostasis might be the result of lipid peroxidation damage. Study demonstrated that hypoxia can cause cellular lipid peroxidation, which in turn can cause inhibition/reduction in the activities of Na+-K+- ATPases. This result can, in turn, affect the intracellular concentrations of Na+,K+, alter the signal transduction pathways, and affect contractility and excitability and cellular dysfunctions such as neuropathy. Lipid peroxidation played an important role in hypoxic brain damage. Inhibition/reduction of lipid peroxidation might be available for anti-hypoxia damage.

Published in:

2009 3rd International Conference on Bioinformatics and Biomedical Engineering

Date of Conference:

11-13 June 2009