Experimental diabetic neuropathy: Role of oxidative stress and mechanisms involved

• Published in: BioFactors (Oxford) 1998, Vol.8 (1-2), p.41-43
• Main Authors: Martínez-Blasco, Amparo, Bosch-Morell, Francisco, Trenor, Carlos, Romero, Francisco J.
• Format: Article
• Language: English
• Subjects: Animals; Blood Glucose - drug effects; Blood Glucose - metabolism; Diabetes Mellitus, Experimental - enzymology; Diabetes Mellitus, Experimental - physiopathology; Diabetic Neuropathies - enzymology; Diabetic Neuropathies - physiopathology; Enzyme Inhibitors - pharmacology; Glutathione Peroxidase - metabolism; Male; Mice; Naphthalenes - pharmacology; Oxidative Stress - physiology; Protein Kinase C - antagonists & inhibitors; Sciatic Nerve - enzymology; Sodium-Potassium-Exchanging ATPase - metabolism
• ISSN: 0951-6433; 1872-8081
• DOI: 10.1002/biof.5520080108

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.