Int J Sports Med 2006; 27(1): 19-24
DOI: 10.1055/s-2005-837506
Physiology & Biochemistry

© Georg Thieme Verlag KG Stuttgart · New York

Alterations in Antioxidant Status, Protein Concentration, Acetylcholinesterase, Na+, K+-ATPase, and Mg2+-ATPase Activities in Rat Brain after Forced Swimming

T. Tsakiris1 , P. Angelogianni1 , C. Tesseromatis2 , S. Tsakiris1 , C. Tsopanakis1
  • 1Department of Experimental Physiology, Medical School, University of Athens, Athens, Greece
  • 2Department of Experimental Pharmacology, Medical School, University of Athens, Athens, Greece
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Publication History

Accepted after revision: November 25, 2004

Publication Date:
09 May 2005 (online)

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Abstract

The aim of this study was to investigate whether exercise stress (short [2 h] or prolonged [5 h] forced swimming in rats) could modulate brain total antioxidant status (TAS), tissue protein concentration, and the activities of acetylcholinesterase (AChE), Na+, K+-ATPase, and Mg2+-ATPase. Protein concentration, TAS and enzyme activities in homogenized rat brain were determined spectrophotometrically. Protein concentration was decreased by 15 % (p < 0.01) and by 30 % (p < 0.001) after 2 h and 5 h of forced swimming, respectively. TAS was decreased by 20 - 25 % after 2 h or 5 h of exercise. AChE was inhibited by 30 % (p < 0.001) and 45 % (p < 0.001) after 2 h and 5 h of forced swimming, respectively. In contrast, Na+, K+-ATPase and Mg2+-ATPase were stimulated by 80 % (p < 0.001) and 40 % (p < 0.001), respectively, after 2 h of swimming and by 100 % (p < 0.001) and 60 % (p < 0.001), respectively, after 5 h of exercise. Control values in nontreated rats were unaltered (p > 0.05). In conclusion, short or prolonged forced swimming induces oxidative stress in rats, probably resulting in a reduction in brain protein concentration and AChE activity. In addition, a Na+, K+-ATPase and Mg2+-ATPase activation was observed under the above mentioned experimental conditions. This stress condition may modulate brain intracellular Mg2+ concentration, neural excitability, metabolic energy production, and neurotransmission.

References

PhD S. Tsakiris

Department of Experimental Physiology, Medical School, University of Athens

P.O. Box 65257

15401 Athens

Greece

Fax: + 30 21 07 46 25 71

Email: stsakir@cc.uoa.gr