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Published on: February 17, 2018
Cardiomyopathy induced by T-2 toxin in rats
Vesna Jaćević1, Qinghua Wu2, Eugenie Nepovimova3
1National Poison Control Centre, Military Medical Academy, 17 Crnotravska St, 11000, Belgrade, Serbia; Medical Faculty of the Military Medical Academy, University of Defence, 1 Pavla Jurišića-Šturma St, 11000, Belgrade, Serbia; Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czech Republic.
Abstract:
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.
Insights
T-2 toxin causes severe heart damage in rats, characterized by myocardial alterations and inflammation. Mast cell degranulation is linked to T-2 toxin-induced cardiomyopathy, offering targets for future treatments.
Area of Science:
- Toxicology
- Cardiovascular Pathology
- Immunology
Background:
- T-2 toxin is an immunotoxic trichothecene mycotoxin with known cardiotoxicity.
- The precise mechanisms underlying T-2 toxin-induced cardiomyopathy remain incompletely understood.
Purpose of the Study:
- To investigate the pathogenesis of T-2 toxin-induced cardiomyopathy in a Wistar rat model.
- To evaluate the temporal effects of T-2 toxin on cardiac tissue, including histopathology and mast cell activity.
Main Methods:
- Cardiomyopathy was induced in Wistar rats via a single subcutaneous injection of T-2 toxin (0.23 mg/kg).
- Cardiac tissues were analyzed using histopathology, semiquantitative scoring (CDS, GDS, VDS), and mast cell quantification at multiple time points (days 1, 7, 14, 21, 28, 60).
Main Results:
- Significant myocardial alterations, irregular glycogen distribution, and hemorrhagic foci were most pronounced on days 28 and 60 post-treatment.
- Diffuse accumulation and degranulation of mast cells (MCs) were observed, correlating negatively with myocardial injury.
- Positive correlations were found between myocardial injury, glycogen distribution, and hemorrhage intensity.
Conclusions:
- T-2 toxin induces significant cardiotoxicity and cardiomyopathy in rats.
- Mast cell degranulation is a key feature in T-2 toxin-induced heart damage.
- These findings are crucial for developing therapeutic strategies against T-2 toxin cardiotoxicity.
