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). The stereological evaluation of glycogen content in histological sections of the heart was processed with periodic acid-Schiff (PAS). Histochemical procedure showed a significant accumulation of glycogen granules in the 3NPA group (0.028mm(3)/mm(3)±0.022), whereas the hearts of control animals were nearly devoid of glycogen granules (0.002mm(3)/mm(3)±0.001). Haematoxylin-eosin histological staining showed diffuse swelling of cardiomyocytes (3NPA=15.989μm ±1.649; saline=13.456μm ± 0.786), loss of cell cross-striations, lower myofibril volume fraction (3NPA=0.3922mm(3)/mm3 ± 0.0230, saline=0.4550mm(3)/mm3 ± 0.0083), and mononuclear infiltration in the interstitial tissue, mostly along the blood vessels. Sirius red staining showed fibrosis of the heart (3NPA=0.0531mm93)/mm(3)±0.0090, saline=0.0135mm(3)/mm3 ± 0.0051). TUNEL staining showed TUNEL-positive cells in the 3NPA group (2.04cells/mm2 ± 0.92) and almost no TUNEL-positive cells in the saline group (0.27cells/mm2 ± 0.14). This experiment shows that 3NPA-induced histopathological changes in the heart are accompanied by a significant accumulation of glycogen granules in cardiomyocytes.
Highlights
The toxin -nitropropionic acid ( NPA) is a well known food contaminating mycotoxin
The NPA-treated rats could be distinguished from the saline-treated controls by the hunched posture, a declined
In the NPA group we found the significant accumulation of glycogen granules in cardiomyocytes ( . mm / mm ± . , n = ) (Figure A), compared with the control group in which only few glycogen granules in the cytoplasm of some cardiomyocytes were visible ( . mm /mm ± . , n = ) (Figure B)
Summary
The toxin -nitropropionic acid ( NPA) is a well known food contaminating mycotoxin It is naturally present in leguminous plants used to feed animals and can poison grazing livestock. October 2011 ment due to mitochondrial stress This effect develops fast and is not limited to the sites of morphological damage [ ]. Mirandola et al [ ] have recently shown that brain and heart mitochondria were generally more sensitive to NPA and Ca +-induced mitochondrial permeability transition than mitochondria from the liver or kidneys. On the other side, preconditioning with NPA has been shown to induce a protective effect against the consequences of brain [ , , ] and heart ischemia [ ]. Our aim was to evaluate histopathological changes and the glycogen content in the heart muscle of experimental rats with NPA-induced striatal lesions
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