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1 Departments of Regulatory Cell Physiology, and 2 Morphological Anatomy, Graduate School of Medical Sciences, 3 Nagoya City University School of Nursing, 4 Department of Health Science, Institute of Natural Sciences, Nagoya City University, Nagoya 467-8601; 5 Department of Physical Therapy, Nagoya University School of Health Sciences, Nagoya 461-8673, Japan; and 6 Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio 43210
We studied whether hydrogen peroxide
(H2O2) at
10 µM activates the ryanodine
receptor and decreases releasable Ca2+ content in the
sarcoplasmic reticulum after fatigue. Exposure of rabbit or frog
skeletal muscle ryanodine receptors to 10 µM H2O2 enhanced channel activity in lipid
bilayers when the redox potential was defined at cis =
220 mV and trans =
180 mV. Channel activation by 10 µM H2O2 was also observed when cis
potential was set at
220 mV without defining trans
potential, but the effect was less. Reduction of trans redox
potential from
180 to
220 mV did not alter channel activity.
H2O2 at 500 µM failed to activate the channel
when the redox potential was not controlled. Stimulation of the frog
muscle fiber for 2 min (50 Hz, a duty cycle of 200 ms/s) decreased
tetanus tension by ~50%. After 1 min, tetanus recovered rapidly to
~70% of control and thereafter slowly approached the control level.
Amplitudes of caffeine- and 4-chloro-m-cresol-induced contractures were decreased after a 60-min rest. The decrease is not
enhanced by exposure to 10 µM H2O2. These
results suggest that H2O2 markedly activates
the ryanodine receptor under the redox control in vitro, but externally
applied H2O2 may not play an important role in
the postfatigue recovery process.
redox potential; single-channel current; calcium content in sarcoplasmic reticulum; catalase; hydrogen peroxide
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