Catalase/superoxide dismutase (SOD) and catalase/paraoxonase (PON) ratios may implicate poor glycemic control.
BACKGROUND
Previous studies suggest that elevated oxidative stress implicates poor glycemic control resulting in the development of diabetic complications. By evaluating the relationship between paraoxonase (PON) and antioxidant enzyme activities and glycemic control in diabetic patients with and without complications, we investigated whether there is a role of PON and/or antioxidant status in glycemic control.


METHODS
A total of 107 patients with type 2 diabetes mellitus (DM) was included in the study. Seventy-five patients had complications including microangiopathy, proliferative retinopathy, and/or nephropathy while 32 had no complications. The control group consisted of 29 age- and sex-matched healthy persons. Serum superoxide dismutase (SOD) and catalase activities were measured according to Sun and Goth, respectively. Basal and salt-stimulated paraoxonase activities and arylesterase activity were determined using the method of Eckerson et al.


RESULTS
There was an increase in the catalase activity and a decrease in the basal and salt-stimulated PON activity of patients when compared with controls, while no significant difference was observed in SOD activity. PON phenotypes had no effect on any parameter in patient and control groups. The ratio of catalase/SOD was 2.44 +/- 7.10 and 0.17 +/- 0.09 in diabetics and controls, respectively (p = 0.004); this was associated with an elevation in HbA1c levels. On the other hand, catalase/PON ratio was also enhanced in diabetic patients (2.8 +/- 5.2), showing a relationship with HbA1c levels compared to controls (0.29 +/- 0.3, p = 0.000).


CONCLUSIONS
The data of this study reveal that enhanced catalase/SOD and catalase /PON ratios that are correlated with HbA1c levels are observed in diabetic patients; thus, these ratios may be used as markers of poor glycemic control and as risk factors in the development of diabetic complications.
Sözmen
E Y
EY
Department of Biochemistry, Ege University School of Medicine, Bornova-Izmir, Turkey. sozmenmed@ege.edu.tr
Sözmen
B
B
Delen
Y
Y
Onat
T
T
D000328:Adult; D000368:Aged; D000975:Antioxidants; D043303:Aryldialkylphosphatase; D001786:Blood Glucose / Q000032:analysis*; D002265:Carboxylic Ester Hydrolases / Q000097:blood; D016022:Case-Control Studies; D002374:Catalase / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000201:enzymology; D003925:Diabetic Angiopathies / Q000097:blood / Q000201:enzymology / Q000209:etiology; D003928:Diabetic Nephropathies / Q000097:blood / Q000201:enzymology / Q000209:etiology; D003929:Diabetic Neuropathies / Q000097:blood / Q000201:enzymology / Q000209:etiology; D003930:Diabetic Retinopathy / Q000097:blood / Q000201:enzymology / Q000209:etiology; D004789:Enzyme Activation / Q000187:drug effects; D004950:Esterases / Q000097:blood* / Q000235:genetics; D005260:Female; D005609:Free Radicals; D006442:Glycated Hemoglobin / Q000032:analysis*; D006031:Glycosylation; D006801:Humans; D015227:Lipid Peroxidation; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010641:Phenotype; D011110:Polymorphism, Genetic; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D013482:Superoxide Dismutase / Q000097:blood*
D000975:Antioxidants; D043303:Aryldialkylphosphatase; D001786:Blood Glucose; D002265:Carboxylic Ester Hydrolases; D002374:Catalase; D004950:Esterases; D005609:Free Radicals; D006442:Glycated Hemoglobin; D008075:Lipoproteins, HDL; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D013482:Superoxide Dismutase; C019734:arylesterase