Chattopadhyay Pronobesh, Islam Johirul, Goyary Danswrang, Agnihotri Amit, Karmakar Sanjev, Banerjee Subham, Singh Lokendra, Veer Vijay
Pharmaceutical Technology Division, Defence Research Laboratory, Tezpur, India
Pharmaceutical Technology Division, Defence Research Laboratory, Tezpur, India.
Toxicol Ind Health. 2016 Mar;32(3):485-92. doi: 10.1177/0748233713503373. Epub 2013 Nov 5.
Our study aimed to determine the cardiac toxicities of T-2 toxin, a representative mycotoxin that frequently contaminates maize, cereals, and other agricultural products, harvested and stored under damp and cold conditions. Dermal exposure to T-2 toxin caused severe cardiotoxicity in experimental Wistar rats. Electrocardiography studies showed the conduction abnormalities including prolongation of the QT and corrected QT interval, shortening of the PR interval, and tachycardia. Biochemical studies also reported the toxicity of T-2 toxin. T-2 toxin induced acute cardiotoxicity in rats and characterized by significant (p < 0.05) elevation of serum troponin I, creatine kinase (CK) isoenzyme MB, CK isoenzyme NAC, and lactate dehydrogenase as compared to control rats. It is concluded that cardiotoxicity effects of T-2 toxin are thought to be due to direct action on electrocardiac potentials and biochemical changes.
我们的研究旨在确定T-2毒素的心脏毒性,T-2毒素是一种典型的霉菌毒素,经常污染在潮湿寒冷条件下收获和储存的玉米、谷物及其他农产品。经皮肤接触T-2毒素会在实验性Wistar大鼠中引起严重的心脏毒性。心电图研究显示出传导异常,包括QT间期和校正QT间期延长、PR间期缩短以及心动过速。生化研究也报告了T-2毒素的毒性。与对照大鼠相比,T-2毒素在大鼠中诱导急性心脏毒性,其特征为血清肌钙蛋白I、肌酸激酶(CK)同工酶MB、CK同工酶NAC和乳酸脱氢酶显著(p < 0.05)升高。得出的结论是,T-2毒素的心脏毒性作用被认为是由于对心电电位的直接作用和生化变化所致。