丙烯酰胺神经损伤后修复过程中神经组织β-葡萄糖醛酸酐酶活力的变化

Changes of β-glucuronidase in repair period of nervous system injured by acrylamide

目的寻找丙烯酰胺诱导的神经损伤后修复过程的敏感生物标志物。方法丙烯酰胺诱导神经损伤模型，在不同恢复期结合神经行为和病理学改变反映周围神经的修复性变，采用紫外分光光度法检测脑、坐骨神经和血清中β-葡萄糖醛酸酐酶（β-G）活力的变化。结果以神经行为和病理改变为依据初步确定丙烯酰胺神经损伤后的自然恢复期为5～6周。恢复32天起，坐骨神经中β-G活力较对照组明显增高，恢复第32天酶活力达55．65±8．15／（ml·h），第40天酶活力达58．45±6．55／（ml·h）（P〈0．01），脑和血清中的β-G活力则变化不明显，但血清与坐骨神经中酶活力的变化趋势有一定的相关性（γ=0．74）。结论周围神经组织中的β-G活力可作为观察丙烯酰胺中毒时周围神经损伤后修复的较为灵敏简便的生化指标，考虑应用于基础研究，血清β-G活力虽然与周围神经损伤修复呈现一定的相关性，但目前数据并不能充分显示其作为人群流行病学调查筛选指标的依据，需深入探讨其人群的可应用性。

Objective To find biomarker in repair of nervous system which is injured by acrylamide. Methods Acrylamide was administered to Wistar rats to establish animal model of neurotoxicity. The neurobehavior and pathologic changes within exposure and recovery period were observed. The activity of β-glucurunidase （β-G） within brain, sciatic nerve and serum was measured by ultraviolet spectrophotometry. Results The neurobehavior and pathologic changes were combined to determine the natural recovery period （4 to 5 weeks）. The activity of β-G in sciatic nerve was increased significantly after five weeks in comparison with the control group. At the 32^nd day and 40^th day of recovery period, those were 55.65 ± 8.15 activity/ml/h and 58.45 ± 6.55 activity/ml/h, respectively（ P 〈 0.01 ）. While the activity of β-G in brain and serum did not change obviously, but the coefficient of β-G activity between serum and sciatic nerve was 0.74. Conclusion The activity of β-G within peripheral nerve could be applied as a sensitive biochemical indicator in repair of peripheral nerve which was injured by acrylamide and maybe considered as an important biomarker in basic medical study. Whether the activity of serum β-G agreed with the crowd screening study required further research.