Cardiomyopathy induced by T-2 toxin in rats

被引:22
|
作者
Jacevic, Vesna [1 ,2 ,3 ]
Wu, Qinghua [3 ,4 ]
Nepovimova, Eugenie [3 ]
Kuca, Kamil [3 ]
机构
[1] Mil Med Acad, Natl Poison Control Ctr, 17 Crnotravska St, Belgrade 11000, Serbia
[2] Univ Def, Mil Med Acad, Med Fac, 1 Pavla Jurisica Sturma St, Belgrade 11000, Serbia
[3] Univ Hradec Kralove, Fac Sci, Dept Chem, Rokitanskeho 62, Hradec Kralove 50003, Czech Republic
[4] Yangtze Univ, Coll Life Sci, 1 Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
T-2; toxin; Cardiotoxicity; Rats; Histopathology; Semiquantitative; Analyses; SKELETAL-MUSCLE INJURY; CARDIAC MAST-CELLS; FULLERENOL NANOPARTICLES; MOLECULAR-MECHANISMS; SATELLITE CELLS; TRICHOTHECENES; DEOXYNIVALENOL; MACROPHAGES; ACTIVATION; MYCOTOXINS;
D O I
10.1016/j.fct.2020.111138
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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.
引用
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页数:8
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