4.5 Article

Plasma lipid peroxidation products and antioxidant enzyme activities in patients with type 2 diabetes mellitus

Journal

ACTA DIABETOLOGICA
Volume 39, Issue 3, Pages 117-122

Publisher

SPRINGER-VERLAG ITALIA SRL
DOI: 10.1007/s005920200029

Keywords

thiobarbituric acid reactive substances; superoxide dismutase; catalase; type 2 diabetes mellitus

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Diabetes is associated with a significant increase in thiobarbituric acid reactive substances (TBARS) which are considered as an index of endogenous lipid peroxidation. The human body has a complex antioxidant defense system that prevents the initiation of free radical chain reactions. We measured plasma TBARS levels, superoxide dismutase (SOD) and catalase (CAT) activities and compared their relation to the metabolic control of diabetes and diabetic microangiopathy. Sixty-four patients (19 men), aged 52.35 +/- 9.31 years with type 2 diabetes mellitus were included in the study. Thirty-six healthy subjects (12 men), aged 51.02 +/- 7.01 years formed the control group. TBARS levels and SOD activity were elevated in the diabetic group when compared with the control group (p<0.001 and p<0.00001, respectively). However CAT activity was significantly decreased in the diabetic group when compared with the control group (p<0.00001). Patients with diabetic nephropathy and retinopathy. but not neuropathy, had elevated TBARS levels but there was no statistically significant difference when compared with diabetic patients without microangiopathy (p>0.05). There was a positive correlation between plasma TBARS levels and SOD activity (r=0.770, p=0.0001) and a negative correlation between plasma TBARS levels and CAT activity (r=-0.482, p=0.0001). There was also a negative correlation between SOD and CAT activities (r=-0.609, p=0.0001). We found significantly elevated TBARS levels in diabetic patients. We did not observe any correlation between TBARS levels and blood glucose and HbA(1c) levels. Elevated TBARS levels and SOD activity and decreased CAT activity may be due to a compensation mechanism of the body.

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