Cardiomyopathy induced by T-2 toxin in rats
Language English Country Great Britain, England Media print-electronic
Document type Journal Article
PubMed
31981685
DOI
10.1016/j.fct.2020.111138
PII: S0278-6915(20)30025-9
Knihovny.cz E-resources
- Keywords
- Analyses, Cardiotoxicity, Histopathology, Rats, Semiquantitative, T-2 toxin,
- MeSH
- Glycogen metabolism MeSH
- Myocytes, Cardiac metabolism MeSH
- Cardiomyopathies chemically induced etiology pathology MeSH
- Cardiotoxicity etiology pathology MeSH
- Mast Cells pathology MeSH
- Myocardium metabolism pathology MeSH
- Rats, Wistar MeSH
- T-2 Toxin toxicity MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Glycogen 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.
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