T-2毒素致低硒低蛋白大鼠心肌损伤实验观察

目的 探讨低硒低蛋白条件下T-2毒素对大鼠心肌的损伤作用以及补硒对该损伤的保护作用。方法 应用人工合成的低硒低蛋白饲料喂养Wistar大鼠，达到低硒状态后(6周)给予T-2毒素，按0．2mg／kg体重隔日灌胃24周，取大鼠心肌组织进行常规HE染色和电镜观察．并利用免疫组化技术检测心肌中的T-2毒素的含量。利用末端标记法检测心肌细胞凋亡发生情况。结果 T-2毒素灌胃组大鼠心肌T-2毒素表达明显，但灌胃各组之间差异不明显；低硒低蛋白组心肌损伤明显重于常硒常蛋白组．补硒保护作用明显。结论 T-2毒素能够在心肌组织中残留。低硒低蛋白能够加重T-2毒素对心肌的损伤作用．补硒能够起到一定的保护作用。

The experiment observation on rat myocardial damage induced by T-2 toxin in deficient of protein and selenium

Objective To discuss the characteristics of rat myocardial damage induced by T-2 toxin in low protein and low selenium and observe the protection of supplementary selenium from this damage.Methods Wistar rat were fed with synthetic feed which was deficient in selenium and protein. After the rat was deficient in selenium(6w), 0.2 mg/kg body weight of T-2 toxin was given by gavage to rat every other day for 24 weeks. Using microscopy and electron-microscopy morphologically observed the lesions of myocardium, the T-2 toxin in myocardium was detected histochemically and the cardiocyte apoptosis was detected by TUNEL.Results The T-2 toxin expression was evident in the myocardium of rat given T-2 toxin by gavage, but there was no difference among different groups. The myocardial damage in the group deficient in protein and selenium was more serious than that in the group adequate in protein and selenium, and supplementary selenium could protect myocardium from damage.Conclusions T-2 toxins can remain in the myocardium.The deficiencies in protein and selenium can aggravate the damage induced by T-2 toxins and supplementary selenium has protective effect.