Cardiomyopathy induced by T-2 toxin in rats
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články
PubMed
31981685
DOI
10.1016/j.fct.2020.111138
PII: S0278-6915(20)30025-9
Knihovny.cz E-zdroje
- Klíčová slova
- Analyses, Cardiotoxicity, Histopathology, Rats, Semiquantitative, T-2 toxin,
- MeSH
- glykogen metabolismus MeSH
- kardiomyocyty metabolismus MeSH
- kardiomyopatie chemicky indukované etiologie patologie MeSH
- kardiotoxicita etiologie patologie MeSH
- mastocyty patologie MeSH
- myokard metabolismus patologie MeSH
- potkani Wistar MeSH
- T-2 toxin toxicita MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- glykogen MeSH
- T-2 toxin MeSH
T-2 toxin, A trichothecenes mycotoxin, is immunotoxic to animals and humans. Although it is highly cardiotoxic, the pathogenesis of cardiomyopathy caused by T-2 toxin is not entirely clear. Hence, in our research, cardiomyopathy was induced by a single injection of T-2 mycotoxin (0.23 mg/kg s.c., 1 LD50) to Wistar rats. The cardiac tissue was carefully examinated by using basic histopathology, semiquantitative (tissue grading score scales) and imaging (a total number of mast cells - MCs) analyses on days 1, 7, 14, 21, 28 and 60 of the study. The most intensive myocardial alterations (cardiac damage score, CDS = 4.20-4.40), irregular glycogen distribution (glycogen distribution score, GDS = 4.07-4.17), haemorrhagic foci (vascular damage score, VDS = 4.57-4.90), diffuse accumulation and degranulation of MCs were observed on day 28 and 60 after treatment (p < 0.001 vs. control and 1st T-2-toxin-treated group, respectively). Besides, statistically significant positive correlations were obtained regarding myocardial injury, glycogen distribution and intensity of haemorrhage, and a negative correlation was found in the case of MCs. Obtained results are essential and crucial for further in vivo experimental studies, including the development of medications able to reduce T-2 toxin-induced cardiotoxicity.
Citace poskytuje Crossref.org