He Qiuyue, Han Manfu, Rao Mingli
Department of Neurology, Shenzhen Red Cross Hospital, Shenzhen 518035, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2002 Jun;20(3):195-6.
To explore the changes of brain energy metabolism following acrylamide (ACR) poisoning.
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.
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).
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.
探讨丙烯酰胺(ACR)中毒后脑能量代谢的变化。
采用酶分析法观察ACR染毒后O1a小鼠和6J小鼠脑内肌酸激酶(CK)、三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)及葡萄糖含量。
O1a小鼠ATP、CK和葡萄糖水平短暂下降,而6J小鼠ATP水平显著下降(1.76μmol/g,P<0.01),与对照组(2.53μmol/g)相比,ADP和AMP升高,葡萄糖降低。中毒组CK活性(1.13μmol/g,P<0.01)低于对照组(3.16μmol/g),且持续5周。
ACR对O1a小鼠的影响轻微且可逆,但对6J小鼠的影响严重且持久。其对势能供应补偿有严重损害,这可能是丙烯酰胺诱导神经元损伤的生化基础。