摘要
目的 对低硒条件下 ,T- 2毒素损伤大鼠心肌的机制进行实验研究 ,探讨克山病的发病原因。方法 采用低硒饲料喂养大鼠 ,用 T- 2毒素亚急性损伤心肌的动物模型 ,应用原位末端标记法和免疫组化技术检测大鼠心肌细胞凋亡和检测心肌中谷胱甘肽过氧化物酶 (GSH- Px)活性。结果 低硒加 T- 2毒素组大鼠心肌损伤较重 ,凋亡细胞检出较多 ,常硒饲料加 T- 2毒素与低硒饲料加 T- 2毒素组均可见心肌坏死 ;这 2个组心肌组织GSH- Px活性降低 ,心肌中可检出凋亡细胞 ;而后者损伤严重。结论 T- 2毒素可使大鼠心肌损伤 ,在低硒条件下 ,这种损伤加重。低硒条件下 ,T- 2毒素损伤大鼠心肌的机制与脂质过氧化和细胞凋亡有关。
Objective To explore the mechanism of myocardial injury by T 2 toxin with selenium-deficiency and the relationship of Keshan disease.Methods Using rats as animal model of selenium deficiency diet and T 2 toxin attack. The glutathione peroxidase (GSH Px) and apoptosis of the myocardial tissue by biochemistry and TUNEL were observed and the level of selenium and GSH Px were compared with different rat groups.Results The damage of rat heart were found both in T 2 toxion with selenium defficiency group and T 2 toxin without selenium defficiency group; The lowest level of GSH Px activity and most numbers of apoptosis cell were found in T 2 toxion with selenium defficiency group. Conclusions T 2 toxin with selenium defficiency can make rat heart damage easily;Lipid peroxidation and apoptosis involved in injury mechanism of myocardial damage. It can give a trail for study the etiology of Keshan disease.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2001年第1期28-30,共3页
Chinese Jouranl of Endemiology
基金
卫生部科学基金资助项目!( 980 13 0 1)
