Carroll P B, Thornton B M, Greene D A
Diabetes. 1986 Nov;35(11):1282-5. doi: 10.2337/diab.35.11.1282.
Decreased glutathione levels in the ocular lens have been invoked as a possible cause for the decreased lenticular Na+-K+-ATPase in diabetes because both are corrected by aldose reductase inhibitors, and the Na+-K+-ATPase is known to be susceptible to oxidation inactivation. Because an analogous Na+-K+-ATPase defect that is prevented by aldose reductase inhibitors has been described in diabetic peripheral nerve, we examined the effect of streptozocin (STZ) diabetes and aldose reductase inhibition on reduced (GSH) and oxidized (GSSG) glutathione levels in crude homogenates of rat sciatic nerve. Neither GSSG nor GSH levels were altered by 2 or 8 wk of untreated diabetes or by aldose reductase inhibition. Because the defect in Na+-K+-ATPase is fully expressed by 4 wk of STZ diabetes, we conclude that altered glutathione redox state plays no detectable role in the pathogenesis of this defect in diabetic peripheral nerve.
眼晶状体中谷胱甘肽水平降低被认为可能是糖尿病患者晶状体中钠钾ATP酶活性降低的原因，因为二者都可被醛糖还原酶抑制剂纠正，且已知钠钾ATP酶易受氧化失活影响。由于在糖尿病周围神经中也描述了一种类似的、可被醛糖还原酶抑制剂预防的钠钾ATP酶缺陷，我们研究了链脲佐菌素（STZ）诱导的糖尿病及醛糖还原酶抑制对大鼠坐骨神经粗匀浆中还原型（GSH）和氧化型（GSSG）谷胱甘肽水平的影响。未经治疗的糖尿病2周或8周以及醛糖还原酶抑制均未改变GSSG和GSH水平。由于STZ诱导的糖尿病4周时钠钾ATP酶缺陷已完全表现出来，我们得出结论，谷胱甘肽氧化还原状态改变在糖尿病周围神经这一缺陷的发病机制中未起可检测到的作用。
