Key result
In murine myocytes, the CAT transgene nullified ADH-amplified ethanol-induced depression of cell shortening and intracellular Ca(2+) transients, as well as reactive oxygen species generation.
Why the study?
Does antioxidant catalase overexpression prevent ADH-associated cardiac contractile depression after acute ethanol exposure in murine myocytes?
Population
Ventricular myocytes from ADH-CAT double transgenic mice, ADH transgenic mice, CAT transgenic mice, and…
Comparison
Acute ethanol exposure (80-640 mg/dl) vs Wild-type FVB myocytes and baseline conditions
Design
Preclinical
Authors
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Supports ADH inhibition research in ethanol cardiotoxicity models; leaves open human translation from transgenic data.
Does antioxidant catalase overexpression prevent ADH-associated cardiac contractile depression after acute ethanol exposure in murine myocytes?
Antioxidant catalase overexpression effectively antagonizes ADH-induced enhanced cardiac depression and stress signaling in response to acute ethanol exposure in murine myocytes.
Zhang et al. (2005) studied Ethanol-induced cardiac depression. Antioxidant catalase (CAT) overexpression vs. ADH, CAT, and wild-type FVB myocytes was evaluated on Cell shortening and intracellular Ca(2+) transients after ethanol exposure. In murine myocytes, the CAT transgene nullified ADH-amplified ethanol-induced depression of cell shortening and intracellular Ca(2+) transients, as well as reactive oxygen species generation.
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