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Suppression of reactive oxygen species production in the anoxia‐tolerant turtle Trachemys scripta
Author(s) -
Milton Sarah L.,
Prentice Howard,
Nayak Gauri,
Kara Laurie,
Kesaraju Shailaja
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1402-a
Subject(s) - reactive oxygen species , oxidative stress , turtle (robot) , hypoxia (environmental) , biology , programmed cell death , microbiology and biotechnology , pharmacology , chemistry , oxygen , biochemistry , apoptosis , ecology , organic chemistry
Hypoxia‐ischemia with reperfusion is know to cause ROS related damage in mammalian systems, yet the anoxia tolerant freshwater turtle is able to survive repeated bouts of anoxia/reoxygenation without apparent damage. While the physiology of anoxia tolerance has been much studied, the adaptations that permit survival of reoxygenation stress have been largely ignored. In this study we examine ROS production in the turtle striatum and in primary neuronal cultures, and examine the effects of adenosine (AD) on cell survival and ROS. Hydroxyl radical formation was measured by the conversion of salicylate to 2,3‐dihydroxybenzoic acid (2,3‐DHBA) using microdialysis; reoxygenation after 1 or 4 hr anoxia did not result in increased ROS production compared to basal normoxic levels, nor did H 2 O 2 increase after anoxia/reoxygenation in neuronally‐enriched cell cultures. Blockade of AD receptors increased both ROS production and cell death in vitro , while AD agonists decreased cell death and ROS. As turtle neurons proved surprisingly susceptible to externally imposed ROS stress (H 2 O 2 ), we propose that the suppression of ROS formation, coupled to high antioxidant levels, is necessary for reoxygenation survival. As an evolutionarily selected adaptation, the ability to suppress ROS formation could prove an interesting path to investigate new therapeutic targets in mammals. Research Support provided by the NIH and the AHA – Florida‐Puerto Rico Affiliate