TOCP诱发OPIDN后鸡神经组织MAP-2的变化

Changes of MAP-2 in nervous system of hens with OPIDN induced by TOCP

目的 探讨微管相关蛋白 2 (MAP -2 )在三邻甲苯磷酸酯 (TOCP)诱发的迟发性神经毒性 (OPIDN)中的含量变化及OPIDN的发病机制。方法 成年罗曼母鸡 18只 ,经口 1次给予TOCP 3 75和 75 0mg kg ,第 2 2天处死动物 ,冷环境下取出大脑、脊髓和坐骨神经 ,匀浆后WesternBlot方法测定MAP 2的含量。结果 TOCP使鸡大脑沉淀中MAP -2在 3 75和 75 0mg/kg组分别升高 2 82 %和 3 60 % ,上清中分别升高 160 %和 2 0 4% ,与对照组相比 ,差异均有显著性 (P <0. 0 1) ;MAP -2在脊髓沉淀中分别降低 5 0 %和 43 % ,脊髓上清中分别降低 2 8%和 5 5 % (P <0 .0 1) ;坐骨神经上清中分别升高 85 %和 3 2 9% (P <0 .0 1) ,坐骨神经沉淀中未检出。结论 TOCP中毒性可引起鸡神经组织中的MAP 2含量发生不同程度改变 ,这种改变可能与TOCP引起的迟发性神经毒性有关。

Objective To investigate the role of microtubulin-associated protein 2(MAP-2) in tri-ortho-cresyl phosphate(TOCP)induced delayed neurotoxicity(OPIDN) and inqu ire the toxic mechanism of OPIDN in human.Methods Eighteen Roma n hens were administered with a single oral dosage of TOCP at 375 or 750 mg/kg.H ens were sacrificed on day 22,the cerebrum,spinal cord and sciatic nerve were di ssected,and homogenized in ice bath,then the levels of MAP-2 were analyzed by w estern blot.Results The results showed that significant changes of MAP-2 existed in nervous system of hens with OPIDN induced by TOCP.In the c erebrum pellet,the level of MAP-2 increased by 282% and 360% in 375 and 750 mg/kg respectively (n=6,P<0.01),in the supernatant of cerebrum, those were 1 60% and 204%(P<0.01); in spinal cord pellet,the reductions were 50% and 43 %,and in supernatant those were 28% and 55% respectively (n=6,P<0.01);in s ciatic nerve supernatant,MAP-2 enhanced 85% and 329% in 375 and 750 mg/kg respe ctively (n=6,P<0.01).In sciatic nerve pellet,the proteins were not examine d.Conclusion The changes of MAP-2 in nervous system may contribute to the occurrence and development of TOCP induced delayed neurotoxicity.