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Updated: Aug 27, 2026

Production and Detection of Reactive Oxygen Species (ROS) in Cancers
Published on: November 21, 2011
Reactive oxygen species cause diabetes-induced decrease in renal oxygen tension
F Palm1, J Cederberg, P Hansell
1Department of Medical Cell Biology, Biomedical Center, Box 571, 751 23 Uppsala, Sweden. Fredrik.Palm@medcellbiol.uu.se
Aims/Hypothesis:
Augmented formation of reactive oxygen species (ROS) induced by hyperglycaemia has been suggested to contribute to the development of diabetic nephropathy. This study was designed to evaluate the influence of streptozotocin (STZ)-induced diabetes mellitus, as well as the effects of preventing excessive ROS formation by alpha-tocopherol treatment, on regional renal blood flow, oxygen tension and oxygen consumption in anaesthetized Wistar Furth rats.
Methods:
Non-diabetic and STZ-diabetic rats were investigated after 4 weeks with or without dietary treatment with the radical scavenger DL-alpha-tocopherol (vitamin E, 5%). A laser-Doppler technique was used to measure regional renal blood flow, whilst oxygen tension and consumption were measured using Clark-type microelectrodes.
Results:
Renal oxygen tension, but not renal blood flow, was lower throughout the renal parenchyma of diabetic rats when compared to non-diabetic control rats. The decrease in oxygen tension was most pronounced in the renal medulla. Renal cellular oxygen consumption was markedly increased in diabetic rats, predominantly in the medullary region. Diabetes increased lipid peroxidation and protein carbonylation in the renal medulla. Treatment with alpha-tocopherol throughout the course of diabetes prevented diabetes-induced disturbances in oxidative stress, oxygen tension and consumption. The diabetic animals had a renal hypertrophy and a glomerular hyperfiltration, which were unaffected by alpha-tocopherol treatment.
Conclusions/Interpretation:
We conclude that oxidative stress occurs in kidneys of diabetic rats predominantly in the medullary region and relates to augmented oxygen consumption and impaired oxygen tension in the tissue.
Insights
Diabetic nephropathy involves increased oxidative stress and oxygen consumption in the kidney medulla. Vitamin E treatment mitigated these effects, but not renal hypertrophy or hyperfiltration.
Area of Science:
- Nephrology
- Endocrinology
- Physiology
Background:
- Hyperglycemia-induced reactive oxygen species (ROS) are implicated in diabetic nephropathy development.
- Understanding the impact of diabetes on renal oxygen dynamics is crucial for therapeutic strategies.
Purpose of the Study:
- To investigate the effects of streptozotocin-induced diabetes on regional renal blood flow, oxygen tension, and consumption in rats.
- To evaluate the protective role of alpha-tocopherol (vitamin E) in preventing diabetes-related oxidative stress and renal oxygen disturbances.
Main Methods:
- Utilized streptozotocin-induced diabetes model in Wistar Furth rats.
- Measured regional renal blood flow using laser-Doppler and oxygen tension/consumption with microelectrodes.
- Administered DL-alpha-tocopherol (vitamin E) to assess its impact on oxidative stress markers and oxygen dynamics.
Main Results:
- Diabetic rats exhibited reduced renal oxygen tension, particularly in the medulla, and increased oxygen consumption.
- Diabetes elevated lipid peroxidation and protein carbonylation in the renal medulla.
- Alpha-tocopherol treatment normalized oxygen tension and consumption, and reduced oxidative stress markers.
- Renal hypertrophy and glomerular hyperfiltration in diabetic rats were not affected by alpha-tocopherol.
Conclusions:
- Oxidative stress in diabetic kidneys, concentrated in the medulla, is linked to increased oxygen consumption and reduced oxygen tension.
- Alpha-tocopherol effectively counteracts diabetes-induced oxidative stress and oxygen dysregulation in the kidney.
- While vitamin E addresses oxidative aspects, it does not impact structural changes like hypertrophy or functional changes like hyperfiltration.
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