Dietary selenium augments sarcoplasmic calcium release and mechanical performance in mice.
BACKGROUND
As an essential trace element selenium plays a significant role in many physiological functions of the organs. It is found within muscles as selenocystein in selenoprotein N, which is involved in redox-modulated calcium homeostasis and in protection against oxidative stress.


METHODS
The effects of two different selenium compounds (selenate and NanoSe in 0.5 and 5 ppm concentration for two weeks) on muscle properties of mice were examined by measuringin vivomuscle performance,in vitroforce insoleus(SOL) andextensor digitorum longus(EDL) muscles and changes in intracellular Ca2+concentration in single fibers fromflexor digitorum brevis(FDB) muscle.. Western-blot analysis on muscle lysates of EDL and SOL were used to measure the selenoprotein N expression. Control mice received 0.3 ppm Se.


RESULTS
While the grip force did not change, 5 ppm selenium diets significantly increased the speed of voluntary running and the daily distance covered. Both forms of selenium increased significantly the amplitude of single twitches in EDL and SOL muscle in a concentration dependent manner. Selenate increased fatigue resistance in SOL. The amplitude of the calcium transients evoked by KCl depolarization increased significantly from the control of 343 ± 44 nM to 671 ± 51 nM in the presence of 0.5 ppm selenate in FDB fibers. In parallel, the rate of calcium release during short depolarizations increased significantly from 28.4 ± 2.2 to 45.5 ± 3.8 and 52.1 ± 1.9 μM/ms in the presence of 0.5 ppm NanoSe and selenate, respectively. In 0.5 ppm concentration both selenium compounds increased significantly the selenoprotein N expression only in EDL muscle.


CONCLUSIONS
Selenium supplementation augments calcium release from the sarcoplasmic reticulum thus improves skeletal muscle performance. These effects are accompanied by the increased selenoprotein N expression in the muscles which could result in increased oxidative stress tolerance in case of long lasting contraction.
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Dóra
D
Bodnár
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Olga
O
Ruzsnavszky
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Tamás
T
Oláh
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Beatrix
B
Dienes
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Ildikó
I
Balatoni
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Éva
É
Ungvári
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Ilona
I
Benkő
Institute of Animal Science, Biotechnology and Nature, Faculty of the Agricultural and Food Sciences and Environmental Management, University of Debrecen, Debrecen, Hungary.
Beáta
B
Babka
Institute of Animal Science, Biotechnology and Nature, Faculty of the Agricultural and Food Sciences and Environmental Management, University of Debrecen, Debrecen, Hungary.
József
J
Prokisch
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
László
L
Csernoch
Department of Physiology, Faculty of Medicine, University of Debrecen, P.O. Box 400, H-4002 Debrecen, Hungary.
Péter
P
Szentesi
Force; Intracellular calcium concentration; Selenium; Selenoprotein; Skeletal muscle