Key result
Exposure of cultured fetal mouse cardiac myocytes to oxygen radicals and oxidants induced cessation of beating and morphological degeneration with increased intracellular calcium.
Population
cultured fetal mouse cardiac myocytes
Design
Preclinical
Authors
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In vitro radical effects on myocytes leave open dominant reperfusion mechanisms in vivo; prospective studies needed before clinical translation.
In cultured fetal mouse myocytes, oxygen radicals and oxidants induce contractile impairment independent of intracellular calcium increases, whereas subsequent morphological hypercontraction is associated with calcium overload, with hydroxyl radicals likely mediating H2O2-induced injury.
Nakamura et al. (1993) studied Reperfusion injury / oxidative stress. Oxygen radicals and oxidants vs. Antioxidants (catalase, dimethylthiourea, deferoxamine) was evaluated on Contractility, morphology, and intracellular Ca2+ concentration. Exposure of cultured fetal mouse cardiac myocytes to oxygen radicals and oxidants induced cessation of beating and morphological degeneration with increased intracellular calcium.
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