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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Cellular redox state protects acetaldehyde-induced alteration in cardiomyocyte function by modifying Ca2+ release
Toshiharu Oba1, Yoshitaka Maeno, Masataka Nagao
1Department of Cell Physiology, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya, Japan. tooba@med.nagoya-cu.ac.jp
American Journal of Physiology. Heart and Circulatory Physiology
|November 6, 2007
Summary
Acetaldehyde disrupts heart calcium handling, contributing to alcoholic cardiomyopathy. The study reveals that cellular redox state influences acetaldehyde
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- Alcoholic cardiomyopathy is linked to acetaldehyde, a toxic metabolite.
- Acetaldehyde disrupts cardiac calcium (Ca2+) handling and excitation-contraction coupling.
- Reactive oxygen species produced by acetaldehyde alter cellular redox potential.
Purpose of the Study:
- To investigate how cellular redox state modulates acetaldehyde-induced Ca2+ handling.
- To determine the effect of acetaldehyde on Ca2+ transient and ryanodine receptor type 2 (RyR2) channel activity.
Main Methods:
- Confocal imaging system to measure Ca2+ transient in isolated rat ventricular myocytes.
- Planar lipid bilayer method to assess single RyR2 channel activity.
- Monochlorobimane fluorometric method to estimate intracellular reduced glutathione levels.
Main Results:
- Acetaldehyde (1-10 microM) increased Ca2+ transient amplitude and area; 100 microM decreased it.
- Reduced intracellular glutathione levels diminished acetaldehyde's effect on Ca2+ transient.
- Acetaldehyde activated RyR2 channel activity at near resting or unfixed redox potentials, but not at reduced or oxidized states.
Conclusions:
- Acetaldehyde acts as an RyR2 activator, disrupting cardiac muscle function.
- Cellular redox potential plays a protective role against acetaldehyde-induced cardiac alterations.
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