Unimpaired energy metabolism in experimental neuropathy induced by p-bromophenylacetylurea.
Unimpaired energy metabolism in experimental neuropathy induced by p-bromophenylacetylurea.
复制标题
对溴苯乙酰脲诱导的实验性神经病中能量代谢未受损。
DOI：
10.1002/mus.880070906
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发表时间：
1984
期刊：
影响因子：
3.4
通讯作者：
Mintz,KP
中科院分区：
文献类型：
--
作者：
Brimijoin,S;Mintz,KP
通过几种方式检查了能量代谢缺陷对对溴苯乙酰脲（BPAU）诱导神经元病理学的贡献。发现BPAU的饱和水溶液对结晶甘油醛-3-磷酸脱氢酶（GAPDH）或磷酸果糖激酶（PFK）的活性没有影响。BPAU（400 mg/kg）致大鼠后肢全瘫，坐骨神经内源性GAPDH和PFK活性正常。内源性烯醇化酶和神经特异性烯醇化酶活性同样不受影响。因此，BPAU神经病变似乎不太可能涉及糖酵解受损。这一结论得到了未能通过喂食丙酮酸（克雷布斯循环的底物）来预防后肢无力的支持。为了检测对其他步骤糖酵解的干扰或氧化磷酸化的损害，测量了三磷酸腺苷（ATP）和磷酸肌酸。发现瘫痪动物神经中高能磷酸盐的量与未处理和溶剂处理对照的神经相同。在从挤压损伤再生的神经中进行了类似的观察。为了测试营业额，ATP和磷酸肌酸测定神经暴露于N2气氛在体外。由于高能磷酸盐在所有组中以相同的速率消失，因此得出结论，BPAU神经病变不会改变能量利用。我们认为，BPAU神经病变的发生机制并不依赖于能量代谢的改变。
The contribution of defective energy metabolism to the induction of neuronal pathology by p‐bromophenylacetylurea (BPAU) was examined in several ways. It was found that a saturated aqueous solution of BPAU had no effect on the activity of crystalline glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) or phosphofructokinase (PFK). In rats with total hindlimb paralysis from treatment with BPAU (400 mg/kg), the endogenous GAPDH and PFK of sciatic nerve showed normal activity. Endogenous enolase and nerve‐specific enolase activities were likewise unaffected. Consequently, it appeared improbable that BPAU neuropathy involves impaired glycolysis. This conclusion was supported by the failure to prevent hindlimb weakness by feeding pyruvate, a substrate for the Krebs cycle. To test for interference with glycolysis at other steps, or for an impairment in oxidative phosphorylation, adenosine triphosphate (ATP) and creatine phosphate were measured. The amounts of high energy phosphates in nerves of paralyzed animals were found to be the same as in nerves of untreated and vehicle‐treated controls. A similar observation was made in nerves regenerating from a crush injury. To test turnover, ATP and creatine phosphate were measured in nerves exposed to an N2atmosphere in vitro. Since the high energy phosphates disappeared at the same rates in all groups, it was concluded that BPAU neuropathy does not alter energy utilization. In our view, BPAU neuropathy arises by a mechanism that does not depend on altered energy metabolism.