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Am J Physiol Cell Physiol (December 30, 2003). doi:10.1152/ajpcell.00388.2003
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Submitted on September 11, 2003
Accepted on December 23, 2003

Acetaldehyde alters Ca2+-release channel gating and muscle contraction in a dose-dependent manner

Toshiharu Oba1* and Yoshitaka Maeno2

1 Regulatory Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan
2 Forensic Medical Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan

* To whom correspondence should be addressed. E-mail: tooba{at}med.nagoya-cu.ac.jp.

We studied whether acetaldehyde, which would be produced by alcohol consumption, impacts ryanodine receptor (RyR) activity and muscle force. Exposure to 50~200 µM acetaldehyde enhanced channel activity of frog RyR and rabbit RyR1 incorporated into lipid bilayers. An increase in acetaldehyde to 1 mM modified channel activity in a time-dependent manner, with a brief activation and then inhibition. Application of 200 µM acetaldehyde to frog fibers increased twitch tension. The maximum rate of rise of tetanus tension was accelerated to 1.5 and 1.74 times the control rate on exposure of fibers to 50 and 200 µM acetaldehyde, respectively. Fluorescence monitoring using Fluo-3 demonstrated that 200-400 µM acetaldehyde induced Ca2+ release from the sarcoplasmic reticulum (SR) in frog muscles. Acetaldehyde at 1 mM inhibited twitch tension by ~12% with an increased relaxation time after a small and transient twitch potentiation. These results suggest that moderate concentrations of acetaldehyde can elicit Ca2+ release from the SR by increasing the open probability of the RyR channel, resulting in increased tension. However, the effects of acetaldehyde at clinical doses (1-30 µM) are unlikely to mediate alcohol-induced acute muscle dysfunction.




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