丙烯酰胺中毒后小鼠脑中肌酸激酶和三磷酸腺苷含量的改变及意义

目的：探讨丙烯酰胺（ACR）中毒后脑能量代谢的改变。方法：采用酶分析法测定Ola鼠和6J鼠脑组织匀浆中肌酸激酶（CK）、三磷酸腺苷（ATP）、二磷酸腺苷（ADP）、腺苷酸（AMP）和葡萄含量。结果：Ola鼠上述指标改变轻微。6J鼠ATP水平明显降低，达1．76μmol/g，与对照组（2．53μmol/g)比较，差异有显著性（P＜0．01）；ADP和AMP增加，葡萄糖降低，脑能量负荷值降低，CK活力明显受到抑制，低达1．13μmol/g，与对照组（3．16μmol/g)比较，差异有显著性（P＜0．01），且持续到第5周不恢复。结论：ACR中毒对Ola鼠脑能量代谢影响轻微且可逆，对6J鼠产生严重影响且持续时间长；脑组织供能代偿潜能损伤重，这种能量代谢的抑制是ACR产生神经元损伤的生化基础。

Effect of acrylamide on creatine kinase and adenosine triphosphate in brain of mice and its significance

OBJECTIVE: To explore the changes of brain energy metabolism following acrylamide (ACR) poisoning. METHODS: Creatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method. RESULTS: ATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks). CONCLUSION: The influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.