Sickles D W, Goldstein B D
Toxicol Lett. 1985 Aug;26(2-3):111-8. doi: 10.1016/0378-4274(85)90154-7.
Acrylamide (ACR) produces a central-peripheral distal axonopathy, via an unknown mechanism. We have investigated the effects of ACR on the activity of enzymes responsible for the oxidation of NADH (NADH-tetrazolium reductase activity, NADH-TR) with quantitative histochemical techniques. Chronic (5- or 10-day) injection of ACR (50 mg/kg/day) resulted in a significant decrease in enzyme activity in soleus motoneurons, which normally have high NADH-TR activity. The NADH-TR activity in motoneurons with low oxidative metabolism was not significantly affected. Retrograde labeling of motoneurons with horseradish peroxidase was diminished by the acrylamide treatment. These data demonstrate an acrylamide-induced change in the oxidative metabolism of certain motoneurons; further study will determine whether oxidative metabolism is the primary site of action of ACR in producing the distal axonopathy.
丙烯酰胺（ACR）通过未知机制引发中枢 - 外周远端轴索性神经病。我们运用定量组织化学技术研究了ACR对负责NADH氧化的酶活性（NADH - 四唑还原酶活性，NADH - TR）的影响。慢性（5天或10天）注射ACR（50毫克/千克/天）导致比目鱼肌运动神经元中的酶活性显著降低，而这些运动神经元通常具有较高的NADH - TR活性。氧化代谢较低的运动神经元中的NADH - TR活性未受到显著影响。丙烯酰胺处理使辣根过氧化物酶对运动神经元的逆行标记减少。这些数据表明丙烯酰胺可引起某些运动神经元氧化代谢的改变；进一步研究将确定氧化代谢是否是ACR产生远端轴索性神经病的主要作用位点。
