中文摘要：

为探明T-2毒素持续染毒后的对虾肌肉中m T-2s的残留规律,及其对对虾的脂溶性成分含量的影响。采用20 d蓄积染毒法获得不同染毒剂量组（0、0.5、1.2、2.4、4.8、12.2 mg/kg饲料）的对虾肌肉组织,采用LC-MS/MS检测经三氟乙酸（TFA）水解处理前后样本中的T-2毒素含量,以T-2增量表示m T-2s含量。同时采用索氏提取法测粗脂肪,HPLC法测VA、VD3和VE含量。结果表明,对虾肌肉经TFA水解处理前未发现游离态T-2毒素,水解后检出T-2毒素,即m T-2s,且其含量与染毒剂量呈正相关。而染毒剂量对不同脂溶性成分含量的影响表现出较大差异。高剂量染毒时,粗脂肪、VA和VD3含量呈显著下降（p〈0.05）,而VE的含量呈波动性变化。低剂量染毒时,粗脂肪、VD3和VE含量显著升高（P〈0.05）,表现出低剂量刺激效应,但是粗脂肪与VA含量与m T-2s呈负相关,可能二者与m T-2s的存在形式有关,此结论为挖掘m T-2s的预警指标提供参考。

英文摘要：

This study explored the content of masked T-2 toxin（m T-2） residues and the effect of this toxin on fat-soluble components in T-2 toxin-exposed muscle tissues of shrimp（Litopenaeus vannamei）.L.vannamei muscle tissues from the groups treated with different doses of T-2 toxin（0,0.5,1.2,2.4,4.8,and 12.2 mg/kg feed） after 20 days of cumulative exposure.Content of the T-2 toxin in the muscle tissues before and after trifluoroacetic acid（TFA） hydrolysis was determined by performing liquid chromatography–tandem mass spectrometry; content of m T-2 was expressed by the increment of T-2 toxin.Crude fat content was determined by using Soxhlet method,and vitamin A（VA）,vitamin D3（VD3）,and vitamin E（VE） content was determined by performing high-performance liquid chromatography.Free T-2 toxin was not detected in shrimp muscle tissues before TFA hydrolysis but was detected after TFA hydrolysis.Moreover,its content was positively correlated with the dose of T-2 toxin administered.Different doses of the T-2 toxin exerted significantly different effects on the content of fat-soluble components.Treatment of shrimps with a high dose of the T-2 toxin significantly decreased crude fat,VA,and VD3 content（p 0.05） but fluctuated VE content.Treatment of shrimps with a low dose of the T-2 toxin significantly increased crude fat,VD3,and VE content（p 0.05）,indicating a low-dose stimulatory effect.Crude fat content was negatively correlated and VA and m T-2 toxin content was positively correlated with the existing form of the T-2 toxin.These results can be used as a reference to determine the indicators of m T-2 toxicity.