1. Hyperketonemia (ketosis), oxidative stress and type 1 diabetes
Sushil K. Jain, Robert McVie, Joseph A. Bocchini 
Pathophysiology 
Volume 13, Issue 3, Pages (August 2006)
DOI: /j.pathophys
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2. Fig. 1
Effect of different concentrations of acetoacetate (AA) on GSH, GSSG, malondialdehyde (MDA) and viscosity levels in red blood cells (RBC). Note an increase in MDA, GSSG and viscosity and decrease in GSH level with increasing AA concentrations. Data are taken from reference [6].
Pathophysiology  , DOI: ( /j.pathophys )
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3. Fig. 2
Level of in vitro oxidizability of LDL+VLDL from normals (N), diabetics (D), normoketonemic (NKD) and hyperketonemic diabetics (HKD). Note a significant (p<0.05) increase in lipoprotein oxidizability in hyperketonemic compared with normoketonemic diabetic subjects. Data are taken from reference [37].
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2006 Elsevier Ireland Ltd Terms and Conditions

4. Fig. 3
The relationship between ketonemia and lipid peroxidation levels in type 1 diabetic patients. Data are taken from reference [38].
Pathophysiology  , DOI: ( /j.pathophys )
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5. Fig. 4
Generation of superoxide radicals by acetoacetate (AA) in a cell-free buffer system. Note a significant cytochrome C reduction by AA but not by β-hydroxybutyrate (BHB). Superoxide radical generation by AA was abolished in the presence of superoxide dismutase (SOD). Data are taken from reference [6].
Pathophysiology  , DOI: ( /j.pathophys )
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6. Fig. 5
Proposed mechanisms of excess oxidative cellular damage in type 1 diabetes. The increase in oxidative stress caused by hyperglycemia and ketosis can contribute to the excess vascular inflammation and vascular disease associated with type 1 diabetes.
Pathophysiology  , DOI: ( /j.pathophys )
Copyright © 2006 Elsevier Ireland Ltd Terms and Conditions