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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 content changes of microtubule-associated protein 2 (MAP-2) in the neurotoxin-induced delayed neurotoxicity (OPIDN) induced by trioctylphosphate (TOCP) and the pathogenesis of OPIDN. Methods Eighteen adult roman hen were given TOCP 3 75 and 75 0 mg orally once. The animals were sacrificed on the 22nd day. The brain, spinal cord and sciatic nerve were removed in cold environment. The content of MAP 2 was determined by Western blot after homogenization. Results Compared with the control group, the levels of MAP-2 in chicken brain pellets increased by 82.02% and 360%, respectively, and the levels of MAP-2 increased by 160% and 20% in the supernatant. MAP 2 decreased by 50% and 43% in spinal cord sedimentation, and decreased by 28% and 55% in spinal cord supernatant (P <0.01) ). The sciatic nerve supernatant increased by 85% and 392% respectively (P <0.01), and was not detected in the sciatic nerve. Conclusion Toxicity of TOCP may cause the changes of MAP 2 in chicken nerve tissue to varying degrees, which may be related to the delayed neurotoxicity induced by TOCP.