title: Diabetic patients without vascular complications display enhanced basal platelet activation and decreased antioxidant status.
abstract: Vascular complications are the leading causes of morbidity and mortality in diabetic patients. The contribution of platelets to thromboembolic complications is well documented, but their involvement in the initiation of the atherosclerotic process is of rising interest. Thus, the aim of the present study was to evaluate basal arachidonic acid metabolism in relation to the redox status of platelets in both type 1 and type 2 diabetic patients, in the absence of vascular complications, as compared with respective control subjects. For the first time, we show that basal thromboxane B(2), the stable catabolite of thromboxane A(2), significantly increased in resting platelets from both type 1 and type 2 diabetic patients (58 and 88%, respectively), whereas platelet malondialdehyde level was only higher in platelets from type 2 diabetic subjects (67%). On the other hand, both vitamin E levels and cytosolic glutathione peroxidase activities were significantly lower in platelets from diabetic patients as compared with respective control subjects. We conclude that platelet hyperactivation was detectable in well-controlled diabetic patients without complications. This abnormality was associated with increased oxidative stress and impaired antioxidant defense in particular in type 2 diabetic patients. These alterations contribute to the increased risk for occurrence of vascular diseases in such patients.
authors.affiliation: Unité mixte de Recherche 585 Institut National de la Santé et de la Recherche Médicale/Institut National des Sciences Appliquées de Lyon, Institute for Multidisciplinary Biochemistry of Lipids, Villeurbanne, France. evelyn.vericel@insa-lyon.fr
authors.forename: Evelyne
authors.initials: E
authors.lastname: Véricel
authors.forename: Caroline
authors.initials: C
authors.lastname: Januel
authors.forename: Martine
authors.initials: M
authors.lastname: Carreras
authors.forename: Philippe
authors.initials: P
authors.lastname: Moulin
authors.forename: Michel
authors.initials: M
authors.lastname: Lagarde
mesh_terms: D000975:Antioxidants / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D003925:Diabetic Angiopathies; D005979:Glutathione Peroxidase / Q000097:blood; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation; D008084:Lipoxygenase / Q000097:blood; D008875:Middle Aged; D015539:Platelet Activation; D010974:Platelet Aggregation / Q000502:physiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000097:blood; D012016:Reference Values; D013929:Thromboxane B2 / Q000097:blood*; D014280:Triglycerides / Q000097:blood; D024502:alpha-Tocopherol / Q000097:blood*
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D002784:Cholesterol; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005979:Glutathione Peroxidase; D006442:Glycated Hemoglobin; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases; D013929:Thromboxane B2; D014280:Triglycerides; D024502:alpha-Tocopherol