OBJECTIVE: Lymphocyte 5'-nucleotidase is sensitive to superoxide anion, and is an indicator of oxidative stress in humans. The aim of this study was to assess the effect of the sulfonylurea drugs gliclazide and glibenclamide on lymphocyte ecto-5'-nucleotidase of type 2 diabetic patients. METHODS: Thirty obese type 2 diabetic patients were treated for three months after randomisation either with gliclazide or glibenclamide. Basic laboratory parameters (glycaemia, fructosamine, C-peptide), plasma malondialdehyde levels (MDA) as well as lymphocyte 5'-nucleotidase activity were determined, for all patients and 16 healthy controls, before and after the treatment. RESULTS: 5'-nucleotidase activity in diabetic patients before treatment with gliclazide was 1.61 +/- 0.16 nmol/min/10(6) lymphocytes, and was significantly (P < 0.01) increased compared with the level in healthy controls. After three months of gliclazide treatment, ecto-5'-nucleotidase activity fell significantly by 47.39% and 36% in unstimulated Con A- and PMA-stimulated lymphocytes, respectively. Glibenclamide treatment had no effect on ecto-5'-nucleo-tidase of type 2 diabetic patients. Glycoregulation was improved, as plasma fructosamine decreased from 53.4 to 42.1 and from 50.5 to 43.4 U/g proteins after gliclazide and glibenclamide treatment, respectively. Plasma MDA levels markedly decreased after gliclazide but not glibenclamide treatment. CONCLUSION: These results show that gliclazide treatment inhibits the activity of lymphocyte ecto-5'-nucleotidase and presumably de-creases the concentration of adenosine at the cell surface. A decrease in 5'-nucleotidase activity and attenuation of adenosine production may be a factor in the protection of tissue injury in type 2 diabetic patients.
OBJECTIVE: Lymphocyte 5'-nucleotidase is sensitive to superoxide anion, and is an indicator of oxidative stress in humans. The aim of this study was to assess the effect of the sulfonylurea drugs gliclazide and glibenclamide on lymphocyte ecto-5'-nucleotidase of type 2 diabeticpatients. METHODS: Thirty obese type 2 diabeticpatients were treated for three months after randomisation either with gliclazide or glibenclamide. Basic laboratory parameters (glycaemia, fructosamine, C-peptide), plasma malondialdehyde levels (MDA) as well as lymphocyte 5'-nucleotidase activity were determined, for all patients and 16 healthy controls, before and after the treatment. RESULTS:5'-nucleotidase activity in diabeticpatients before treatment with gliclazide was 1.61 +/- 0.16 nmol/min/10(6) lymphocytes, and was significantly (P < 0.01) increased compared with the level in healthy controls. After three months of gliclazide treatment, ecto-5'-nucleotidase activity fell significantly by 47.39% and 36% in unstimulated Con A- and PMA-stimulated lymphocytes, respectively. Glibenclamide treatment had no effect on ecto-5'-nucleo-tidase of type 2 diabeticpatients. Glycoregulation was improved, as plasma fructosamine decreased from 53.4 to 42.1 and from 50.5 to 43.4 U/g proteins after gliclazide and glibenclamide treatment, respectively. Plasma MDA levels markedly decreased after gliclazide but not glibenclamide treatment. CONCLUSION: These results show that gliclazide treatment inhibits the activity of lymphocyte ecto-5'-nucleotidase and presumably de-creases the concentration of adenosine at the cell surface. A decrease in 5'-nucleotidase activity and attenuation of adenosine production may be a factor in the protection of tissue injury in type 2 diabeticpatients.