Effects of resveratrol on nucleotide degrading enzymes in streptozotocin-induced diabetic rats

Aims: Diabetes mellitus is associated with platelet alterations that may contribute to the development of cardiovascular complications The present study investigates the effects of resveratrol (RSV), an important compound with cardioprotective activities, on NTPDase, ecto-nucleotide pyrophosphatase/phosphodiesterase (E-NPP), 5'-nucleotidase and adenosine deaminase (ADA) activities in platelets from streptozotocin (STZ)-induced diabetic rats. Main methods: The animals were divided into six groups (n=8): control/saline; control/RSV 10 mg/kg; control/RSV 20 mg/kg: diabetic/saline; diabetic/RSV 10 mg/kg; diabetic/RSV 20 mg/kg. RSV was administered during 30 days and after this period the blood was collected for enzymatic assay. Key findings: The results demonstrated that NTPDase, E-NPP and 5'-nucleotidase activities were significantly higher in the diabetic/saline group (P<0.05) compared to control/saline group. Treatment with RSV significantly increased NTPDase, 5'-nucleotidase and E-NPP activities in the diabetic/RSV10 and diabetic/RSV20 groups (P<0.05) compared to diabetic/saline group. When RSV was administered per se there was also an increase in the activities of these enzymes in the control/RSV10 and control/RSV20 groups (P<0.05) compared to control/saline group. ADA activity was significantly increased in the diabetic/saline group (P<0.05) compared to control/saline group. The treatment with RSV prevented this increase in the diabetic/RSV10 and diabetic/RSV20 groups. No significant differences in ADA activity were observed in the control/RSV10 and control/RSV20 compared to control/saline group. Significance: The present findings demonstrate alterations in nucleotide hydrolysis in platelets of STZ-induced diabetic rats and treatment with RSV was able to modulate adenine nucleotide hydrolysis, which may be important in the control of the platelet coagulant status in diabetes. (C) 2009 Elsevier Inc. All rights reserved.