三邻甲苯磷酸酯染毒的母鸡脊髓中AKT/mTOR/p70S6K信号通路的变化  

The changes of AKT/mTOR/p70S6K signaling pathway in spinal cords of hen treated with tri-ortho-cresyl phosphate

作　　者：寇蕊蕊[1] 邹朝双[1] 高媛[1] 谢克勤[1] 宋福永[1] 

机构地区：[1]山东大学公共卫生学院毒理学研究所,山东济南250012

出　　处：《毒理学杂志》2013年第3期157-160,共4页Journal of Toxicology

基　　金：国家自然科学基金(30972498);山东省中青年科学家科研奖励基金(BS2009SW017)

摘　　要：目的研究三邻甲苯磷酸酯(TOCP)所致迟发性神经病(OPIDN)中AKT/mTOR/p70S6K信号通路的变化,探讨OPIDN发生的分子机制。方法 30只成年罗曼母鸡随机分为5组,每组6只,给予750 mg/kg TOCP一次性灌胃,然后分别在TOCP染毒后0、1、5、10和21 d时间点处死一组动物取脊髓组织,免疫印迹法检测脊髓中AKT、p-AKT、p70S6K、p-p70S6K和mTOR的相对含量。结果 TOCP染毒引起母鸡脊髓中磷酸化AKT、p70S6K和mTOR的含量显著下降(P<0.05),而AKT、p70S6K的含量没有明显变化(P>0.05)。结论 TOCP干扰了AKT/mTOR/p70S6K信号通路的调节机制,这可能与OPIDN的发病机制有关。Objective To study the changes of AKT/mTOR/p70S6K signaling pathway in the delayed neuropathy （OPIDN） induced by three-ortho-cresyl phosphate （TOCP） , and explore the molecular mechanism of OPIDN. Methods Thirty adult Roman hens were randomly divided into groups of control, 1 d, 5 d, 10 d and 21 d （6 hens per group）. Except the group control, the rest groups were intoxicated with TOCP by garage at a single dosage of 750 mg/kg. The levels of AKT, p-AKT, p70S6K, p-p70S6K and roTOR in spinal cords were determined by immunoblotting. Results Compared to the control, our results demonstrated a significant decrease in p-AKT, p-p70S6K and roTOR after dosing TOCP（P 〈 0. 05）. However, there was no statistical significance in the level of AKT and p70S6K （P 〉0.05 ）. Conclusion The intoxication of TOCP interferes with the regulatory mechanism of AKT/mTOR/pTOS6K signaling, which might be involved in the pathogenesis of OPIDN.

关 键 词：三邻甲苯磷酸酯 有机磷化合物诱发的迟发性神经病 AKT mTOR p70S6K信号通路 

分 类 号：R114[医药卫生—卫生毒理学]