Skip Navigation

Integrative and Comparative Biology 2002 42(3):463-468; doi:10.1093/icb/42.3.463
© 2002 by The Society for Integrative and Comparative Biology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Lutz, P. L.
Right arrow Articles by Prentice, H. M.
Right arrow Search for Related Content
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Sensing and Responding to Hypoxia, Molecular and Physiological Mechanisms1

Peter L. Lutz2,1 and Howard M. Prentice2
1 Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida 33431
2 Department of Biomedical Sciences, Florida Atlantic University, Boca Raton, Florida 33431

In order to adapt to low oxygen it is necessary first to be able to detect hypoxia, then to initiate the appropriate defense mechanisms. There are two basic detectors: molecular sensors that are directly linked to gene regulation and metabolic indicators that are triggered when the cell goes into a state of energy imbalance. The molecular responses to oxygen deprivation are characterized in a variety of cell types and include activation of oxygen sensors, signaling through specific promoter elements and subsequent downstream adaptations. Many of the components are highly conserved across species. In the brain, the most hypoxic vulnerable of all vertebrate tissues, low oxygen quickly results in a fall in ATP and a consequent increase in adenosine. Both changes act as metabolic indicators of cellular energy crisis and effect mechanisms to reduce metabolic demand. Important lessons on the potential scope of such mechanisms can be provided by the anoxic tolerant turtle brain. Anoxia provokes an early release of adenosine which mediates channel arrest, causes a reduction in K+ efflux and Ca2+ influx, and inhibits excitatory neurotransmitter release. There is a differential expression between normoxic and anoxic turtle brains of transcripts encoding the immediate early gene products c-fos and c-jun, the HSP-70 and the apoptosis regulators bcl-2 and bax.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Integr. Comp. Biol.Home page
M. E. Feder
Plant and Animal Physiological Ecology, Comparative Physiology/Biochemistry, and Evolutionary Physiology: Opportunities for Synergy: An Introduction to the Symposium
Integr. Comp. Biol., July 1, 2002; 42(3): 409 - 414.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.