National 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.
College of Life Science, Yangtze University, 1 Nanhuan Road, 434023, Jingzhou, Hubei, China; Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czech Republic.
Food Chem Toxicol. 2020 Mar;137:111138. doi: 10.1016/j.fct.2020.111138. Epub 2020 Jan 22.
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 LD) 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.
T-2 毒素是一种单端孢霉烯族真菌毒素，对动物和人类具有免疫毒性。尽管它具有高度的心脏毒性，但 T-2 毒素引起心肌病的发病机制尚不完全清楚。因此，在我们的研究中，通过单次注射 T-2 真菌毒素（0.23mg/kg，皮下注射，1LD）诱导 Wistar 大鼠发生心肌病。使用基本组织病理学、半定量（组织分级评分量表）和成像（总肥大细胞数量 - MCs）分析，在研究的第 1、7、14、21、28 和 60 天仔细检查心脏组织。在治疗后第 28 天和第 60 天观察到最剧烈的心肌改变（心肌损伤评分，CDS=4.20-4.40）、不规则糖原分布（糖原分布评分，GDS=4.07-4.17）、出血灶（血管损伤评分，VDS=4.57-4.90）、MC 弥漫性聚集和脱颗粒（p<0.001，与对照组和第 1 次 T-2 毒素处理组相比）。此外，在心肌损伤、糖原分布和出血强度方面观察到统计学上显著的正相关，而在 MCs 方面则存在负相关。获得的结果对于进一步的体内实验研究至关重要，包括开发能够减轻 T-2 毒素引起的心脏毒性的药物。
