Affiliations: Experimental Toxicology and Neurotoxicology Unit, Department of Physiology, School of Medicine and Dentistry, University of Valencia, 46010 Valencia, Spain
Note: [] Correspondence to: Prof. Dr. Francisco J. Romero, Department of Physiology, School of Medicine and Dentistry, University of Valencia, Av. Blasco Ibañez, 17, 46010 Valencia, Spain. Tel.: +34 6 386 4646; Fax: +34 6 386 4173; E‐mail: Fco.Romero@ uv.es.
Abstract: Oxidative stress has been related to the development of diabetic neuropathy. Experimental diabetes (alloxan injection to 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 diabetic 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.
Journal: Biofactors, vol. 8, no. 1-2, pp. 41-43, 1998
