摘要
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O1a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)和葡萄糖含量。结果O1a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。
Objective To explore the changes of brain energy metabolism following acry lamide(ACR)poisoning.Meth ods creatie kinase(CK),adenosine triphosphate(ATP),adenosine diphosphate(ADP),adenosine5'-monophosphate(AMP)and glucose contents in brain were observed in O1a mice and6J mice following ACR intox-ication by enzyme analytical method.Re sults ATP,CK and glucose levels decreased transiently in O1a mice,while ATP level in6J mice was significantly decreased(1.76μmol/g,P<0.01),as compared to the control(2.53μmol/g)but ADP and AMP were increased,glucose was decreased.The activity of CK in poisoned group(1.13μmol /g,P<0.01)was lower than that of control(3.16μmol /g and lasted for5weeks).Con clu sion The in-fluence of ACR on Ola mice was slight and reversible but on6J mice was severe and lasting.There was sereve damage to the potential energy supply compensation,which might be the biochemical basis of neuron damage induced by acrylamide.[
出处
《中华劳动卫生职业病杂志》
CAS
CSCD
北大核心
2002年第3期195-198,共4页
Chinese Journal of Industrial Hygiene and Occupational Diseases
