T-2毒素及其对关节软骨和心肌毒性研究进展  

Pathogenic Mechanism of T-2 Toxin for Kashin-Bek Syndrome and Keshan Disease

作　　者：周晓菲[1] 冯晓声[1] 张乃生[1] 周昌芳[1] 冯晓群[1] 

机构地区：[1]吉林大学畜牧兽医学院,吉林长春130062

出　　处：《动物医学进展》2006年第12期49-53,共5页Progress In Veterinary Medicine

摘　　要：T-2毒素是A族单端孢霉烯族毒素中毒性最强的毒素,也是我国两种地方病,即大骨节病和克山病最可能的致病因素,主要对关节软骨及心肌有毒害作用。T-2毒素可以诱导细胞凋亡,引起家畜、家禽关节超微结构的改变和关节软骨细胞的损伤;还能影响心肌离子通道电活动,影响脂质过氧化物代谢,也能改变心肌超微结构;微量元素硒对T-2毒素致关节软骨和心肌损害有明显的保护作用。大骨节病和克山病的高发地区粮食中T-2毒素含量偏高20%左右,所以大骨节病和克山病可能和T-2毒素中毒有关。T-2 toxin is the one fortised toxin in A group trichotheceneae, toxication to T-2 toxin is the most probable etiopathogenisis of Kashin-Bek syndrome and Keshan disease. T-2 toxin may poison arthrodial cartilage and cardiac muscle. T-2 toxin may induce cell apoptosis and damage the arthrodial cartilage, change the arthrodial ultrastructue, effect electric activity in ion channel of cardiac muscle and metabolism of the lipid peroxidation, change uhrastructue the of cardiac muscle. Element Se can protect arthrodial cartilage and cardiac muscle from T-2 toxin. The content of T-2 toxin is higher about 20% in foodstuff in the places where Kashin-Beck disease and Keshan disease occur.

关 键 词：T-2毒素 大骨节病 克山病 

分 类 号：S859.82[农业科学—临床兽医学] S859.87[农业科学—兽医学]