Reduced glutathione concentrations are not decreased in red blood cells of patients with long term type 1-diabetes

Abstract

Aims/hypothesis. Glutathione is a major part of the intracellular antioxidant defence against reactive oxygen species (ROS). We aimed to study the erythrocyte concentrations of reduced glutathione (GSH) and oxidized glutathione (GSSG) in patients with long term type 1-diabetes and normal kidney function compared to a control group. Methods. Fasting erythrocyte concentrations of GSH and GSSG were measured by HPLC with column switching. Results. Fifty-nine patients with type 1-diabetes for 26 (10.7) years, mean (SD) with a HbA_1c of 7.8 (0.9) % and normal concentrations of S-creatinine were compared with 57 age- and sex-matched healthy controls. GSH (μmol/g protein) concentrations were 5.25 (4.59–6.23) (median and 95% CI) in the control group vs. 5.12 (4.43–5.99) in the diabetes group (p = 0.39). GSSG (μmol/g protein) concentrations were 0.092 (0.063–0.179) in the control group vs. 0.138 (0.067–0.247) in the diabetes group (p = 0.15). Concentrations of GSH correlated with diabetes duration (r = 0.36, p < 0.01) and serum concentrations of methylglyoxal-derived hydroimidazolone MG-H1 (r = 0.41; p < 0.005). In the control group, GSH correlated with MG-H1 (r = 0.27; p < 0.05). In a multiple regression analysis in the diabetes group with GSH as the dependent variable; the significant independent variables were MG-H1 (p = 0.001) and diabetes duration (p = 0.008). Conclusions/interpretation. Despite a significant positive association between GSH and methylglyoxal-derived hydroimidazolone MG-H1 and diabetes duration the concentrations of GSH and GSSG in erythrocytes did not differ between patients with type 1-diabetes and controls.

Key Words::

• Glutathione
• diabetes
• erythrocytes
• methylglyoxal-derived hydroimidazolone MG-H1

Acknowledgements

We thank Aase-Brith Jensen for technical assistance in the measurement of S-methylglyoxal-derived hydroimidazolone MG-H1.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.