Relationship between anoxia exposure and antioxidant status in the frog rana pipiens. Hermes-Lima, Marcelo, and Kenneth B. Storey. Institute of Biochemistry and Department of Biology, Carleton University, Ottawa, ON, K1S 5B6 Canada (FAX: 613-520-4389) & Departamento de Biologia Celular, Universidade de Brasilia, Brasilia, DF, 70.910-900 Brazil
APStracts 3:0130R, 1996.
The biochemical adaptations of cellular antioxidant defenses that permit anoxia-tolerant animals to deal effectively with rapid and large changes in oxygen availability, and hence oxidative stress, during transitions from anoxia to normoxia provide insights into the strategies of antioxidant defense that could help to minimize reperfusion injuries to mammalian organs following anoxia/ischemia stress. The present study analyzes the effects of 30 h anoxia exposure followed by reoxygenation on the antioxidant defenses (activities of five enzymes, glutathione status) and lipid peroxidation damage to organs of the leopard frog Rana pipiens (5 C -adapted autumn frogs). Exposure to 30 h anoxia resulted in significant increases in the activities of skeletal muscle and heart catalase (by 53% and 47%), heart and brain glutathione peroxidase (GPX) (by 75% and 30%), and brain glutathione S-transferase (by 66%). In most cases, enzyme activities had returned to the control values following 40 h aerobic recovery. Activities of superoxide dismutase and glutathione reductase were unaltered in any of the organs and anoxia/recovery had no effect on any of the enzymes in liver. Glutathione equivalents (GSH-eq) were maintained in four organs during anoxia but decreased by 32% in brain during anoxia. Brain GSH -eq had recovered after 90 min reoxygenation and, in addition, hepatic GSH-eq rose by 71% after 90 min reoxygenation. The ratio GSSG/GSH-eq was also affected by anoxia in an organ-specific way. Lipid peroxidation, assessed as the content of thiobarbituric acid reactive substances (TBARS), was unaltered in skeletal muscle and liver following 30 h anoxia exposure or short (25 & 90 min) or long term (40 h) periods of reoxygenation indicating that cycles of natural and survivable anoxia/reoxygenation occur without significant increase in TBARS in selected organs. Overall, the data demonstrate that elements of the antioxidant system of R. pipiens are induced during anoxia exposures as a possible preparation for dealing with potentially harmful oxygen reperfusion stress. 

Received 7 June 1995; accepted in final form 27 March 1996.
APS Manuscript Number R342-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 16 April 96