6533b826fe1ef96bd1285227

RESEARCH PRODUCT

Experimental diabetic neuropathy: role of oxidative stress and mechanisms involved.

Amparo Martínez-blascoCarlos TrenorFrancisco J. RomeroFrancisco Bosch-morell

subject

Blood GlucoseMalemedicine.medical_specialtyDiabetic neuropathyClinical BiochemistryNaphthalenesmedicine.disease_causeBiochemistryDiabetes Mellitus Experimentalchemistry.chemical_compoundMiceDiabetic NeuropathiesGlycationInternal medicineAlloxanmedicineAnimalsEnzyme InhibitorsProtein kinase CProtein Kinase CGlutathione Peroxidasebusiness.industryNervous tissueGeneral MedicineGlutathionemedicine.diseaseSciatic NerveOxidative Stressmedicine.anatomical_structureEndocrinologychemistryMolecular MedicineSciatic nerveSodium-Potassium-Exchanging ATPasebusinessOxidative stress

description

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.

yearjournalcountryeditionlanguage
1998-08-12BioFactors (Oxford, England)
10.1002/biof.5520080108https://pubmed.ncbi.nlm.nih.gov/9699007