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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.
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