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Experimental diabetic neuropathy: role of oxidative stress and mechanisms involved
A Martínez-Blasco1, F Bosch-Morell, C Trenor
1Department of Physiology, School of Medicine and Dentistry, University of Valencia, Spain.
Abstract:
Oxidative stress has been related to the development of diabetic neuropathy. Experimental diabetes (alloxan injection of 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 diabetes 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.
Insights
In diabetic mice, inhibiting protein kinase C (PKC) did not restore glutathione peroxidase (GSHPx) activity in sciatic nerves. This suggests protein glycation, not PKC, may be an early cause of GSHPx changes in diabetic neuropathy.
Area of Science:
- Neuroscience
- Biochemistry
- Endocrinology
Background:
- Diabetic neuropathy is linked to oxidative stress and early biochemical changes in peripheral nerves.
- Experimental diabetes in mice shows decreased Na,K-ATPase and glutathione peroxidase (GSHPx) activity.
- Protein kinase C (PKC) activation is observed in experimental diabetes, and its inhibition can restore Na,K-ATPase activity.
Purpose of the Study:
- To investigate the role of PKC inhibition on GSHPx activity in the sciatic nerve of diabetic mice.
- To determine if PKC inhibition can reverse early biochemical changes in diabetic neuropathy.
Main Methods:
- Induction of experimental diabetes in mice using alloxan.
- Inhibition of PKC at 4 days post-alloxan administration.
- Measurement of GSHPx activity in the sciatic nerve tissue.
Main Results:
- PKC inhibition did not restore GSHPx activity to normal levels in the sciatic nerves of diabetic mice.
- This finding contrasts with the known effect of PKC inhibition on Na,K-ATPase activity.
Conclusions:
- PKC does not appear to control GSHPx activity in the sciatic nerve during early experimental diabetes.
- The results support the hypothesis that protein glycation may be an earlier event affecting GSHPx in diabetic neuropathy.