[HTML][HTML] Glycogen accumulation in cardiomyocytes and cardiotoxic effects after 3NPA treatment

A Milutinović, R Zorc-Pleskovič - Bosnian Journal of Basic Medical …, 2012 - ncbi.nlm.nih.gov
A Milutinović, R Zorc-Pleskovič
Bosnian Journal of Basic Medical Sciences, 2012ncbi.nlm.nih.gov
Abstract Mitochondrial toxin 3-nitropropionic acid (3NPA) is a neurotoxin that inhibits the
activity of succinate dehydrogenase, a key enzyme of oxidative energy production, and
characteristically provokes neurodegeneration in the striatum, resembling Huntington's
disease. 3NPA also affects the activity of glycogen-sinthase-kinase-3b (GSK-3b), an enzyme
implicated in glycogen synthesis and in signal transduction. The aim of this study was to
evaluate cardiac glycogen content and histopathological changes in the hearts of rats after …
Abstract
Mitochondrial toxin 3-nitropropionic acid (3NPA) is a neurotoxin that inhibits the activity of succinate dehydrogenase, a key enzyme of oxidative energy production, and characteristically provokes neurodegeneration in the striatum, resembling Huntington’s disease. 3NPA also affects the activity of glycogen-sinthase-kinase-3b (GSK-3b), an enzyme implicated in glycogen synthesis and in signal transduction. The aim of this study was to evaluate cardiac glycogen content and histopathological changes in the hearts of rats after subchronic treatment with 3NPA. Female adult Wistar rats were treated daily with 30mg/kg of 3NPA subcutaneously 8 days. The control group was treated with normal saline for 8 days. For the comparison of measured parameters between groups we used the Student’s t-test (p< 0.05).
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