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- Title
Glutathione redox state is not the link between polyol pathway activity and myo-inositol-related Na+-K+-ATPase defect in experimental diabetic neuropathy.
- Authors
Carroll, P. B.; Thornton, B. M.; Greene, D. A.
- Abstract
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.
- Publication
Diabetes, 1986, Vol 35, Issue 11, p1282
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diabetes.35.11.1282