Jackson G R, Apffel L, Werrbach-Perez K, Perez-Polo J R
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston 77550.
J Neurosci Res. 1990 Mar;25(3):360-8. doi: 10.1002/jnr.490250313.
The nerve growth factor protein (NGF) regulates neuronal cell death during the development of embryonic sensory and sympathetic neurons in the peripheral nervous system (PNS). NGF protects the rat pheochromocytoma line PC12, a useful model of NGF responsive peripheral neurons, from hydrogen peroxide, which interacts with ferrous iron to generate hydroxyl radicals. Exogenous catalase provides protection, whereas superoxide dismutase (SOD) has no effect on neuronal survival when PC12 cells are challenged with hydrogen peroxide. NGF treatment of PC12 cells increases the activity of catalase. NGF protection from hydrogen peroxide is partially abolished by aminotriazole (Az), a low molecular weight catalase inhibitor. Taken together, these data are consistent with the hypothesis that NGF protects from peroxidative events and consequent cell death via an induction of free radical detoxifying mechanisms, such as catalase activity.
神经生长因子蛋白（NGF）在周围神经系统（PNS）胚胎感觉神经元和交感神经元发育过程中调节神经元细胞死亡。NGF保护大鼠嗜铬细胞瘤细胞系PC12（一种对NGF有反应的周围神经元的有用模型）免受过氧化氢的损伤，过氧化氢与亚铁离子相互作用产生羟基自由基。当PC12细胞受到过氧化氢攻击时，外源性过氧化氢酶可提供保护，而超氧化物歧化酶（SOD）对神经元存活没有影响。用NGF处理PC12细胞可增加过氧化氢酶的活性。低分子量过氧化氢酶抑制剂氨基三唑（Az）可部分消除NGF对过氧化氢的保护作用。综上所述，这些数据与以下假设一致：NGF通过诱导自由基解毒机制（如过氧化氢酶活性）来保护细胞免受过氧化事件及随之而来的细胞死亡。
