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Glutathione and its redox system in diabetic polymorphonuclear leukocytes
The American Journal of the Medical Sciences
|May 1, 1984
Summary
Diabetic polymorphonuclear leukocytes show reduced glutathione levels and impaired glutathione peroxidase activity. Insulin treatment significantly restored these glutathione system functions in diabetic patients.
Area of Science:
- Biochemistry
- Immunology
- Diabetology
Background:
- Diabetic complications are often linked to oxidative stress.
- Polymorphonuclear leukocytes (PMNs) play a crucial role in immune response and are susceptible to oxidative damage.
- Glutathione is a key intracellular antioxidant crucial for cellular defense.
Purpose of the Study:
- To investigate the status of the glutathione system in polymorphonuclear leukocytes (PMNs) of diabetic patients.
- To determine the impact of ketosis on the glutathione system in diabetes.
- To assess the effect of insulin therapy on PMN glutathione levels and activity.
Main Methods:
- Quantification of reduced glutathione levels in PMNs.
- Measurement of glutathione reductase and glutathione peroxidase activities in PMNs.
- Comparison between diabetic patients (with and without ketosis) and healthy controls.
- Evaluation of PMNs from insulin-treated diabetic patients.
Main Results:
- Significantly decreased levels of reduced glutathione were observed in diabetic PMNs compared to normal.
- Glutathione peroxidase activity was significantly reduced in diabetic PMNs, while glutathione reductase activity remained unchanged.
- Ketosis did not exacerbate the observed alterations in the glutathione system.
- Insulin treatment led to a significant restoration of glutathione levels and enzyme activities in PMNs.
Conclusions:
- Diabetic polymorphonuclear leukocytes exhibit a compromised glutathione system, characterized by reduced glutathione and impaired glutathione peroxidase activity.
- The observed glutathione system dysfunction in diabetes is potentially reversible with insulin therapy.
- These findings highlight the role of the glutathione system in diabetic immune cell function and suggest therapeutic implications.