Martínez-Blasco A, Bosch-Morell F, Trenor C, Romero F J
Department of Physiology, School of Medicine and Dentistry, University of Valencia, Spain.
Biofactors. 1998;8(1-2):41-3. doi: 10.1002/biof.5520080108.
Oxidative stress has been related to the development of diabetic neuropathy. Experimental diabetes (alloxan injection of mice) promotes early biochemical changes in peripheral nervous tissue, e.g. decrease in Na,K-ATPase activity and glutathione (GSH) peroxidase (GSHPx) activity. The former decrease can be reverted by inhibiting protein kinase C (PKC), since it has been reported that PKC is activated in these experimental conditions. Here we present data demonstrating that the inhibition of PKC, as early as 4 days after alloxan administration, is not able to return to normal values GSHPx activity in sciatic nerve of diabetes mice. Thus, it would fit with our previous proposal of the possible glycation of this protein as an early event in experimental diabetes, and apparently rules out the control of GSHPx activity by PKC in this tissue.
氧化应激与糖尿病神经病变的发生有关。实验性糖尿病（给小鼠注射四氧嘧啶）会促使周围神经组织早期发生生化变化，例如钠钾-ATP酶活性和谷胱甘肽（GSH）过氧化物酶（GSHPx）活性降低。前者的降低可通过抑制蛋白激酶C（PKC）来逆转，因为据报道在这些实验条件下PKC会被激活。在此我们展示的数据表明，在给小鼠注射四氧嘧啶4天后尽早抑制PKC，并不能使糖尿病小鼠坐骨神经中的GSHPx活性恢复到正常水平。因此，这与我们之前提出的该蛋白可能发生糖基化作为实验性糖尿病早期事件的观点相符，并且显然排除了PKC对该组织中GSHPx活性的调控作用。
