Analysis of the interaction between hyperglycemia and oxidative stress on immune cells of patients with type 2 diabetes.

LAGUARDE NATALIA; GEREZ ESTHER; WALD MIRIAM; SERRA ALEJANDRO; TORRACO LLANES MARTÍN; FRECHTEL GUSTAVO

Congreso; XLVIII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE FARMACOLOGÍA EXPERIMENTAL; 2016

SAIC

Diabetics are predisposed to infections, suggesting an association between diabetes and immunosuppression, being hyperglycemia the main factor involved. High glucose (HG) induces reactive oxygen species (ROS) and oxidative stress is involved in the pathophysiology. However, there are patients who recover normally from infections. Genetic conditioning could be a factor involved. In a previous work we observed that lymphocytes isolated from BALB/c mice were sensitive to the deleterious effect of hyperglycaemia, while C57 were resistant. Oxidative stress was implicated in this deleterious effect. In the present study we start to analyze the interaction between hyperglycemia and oxidative stress on immune cells in type 2 diabetic patients (D2). Antioxidant status was estimated by measuring glutathione content (GSH) and oxidative stress by measuring ROS generation in lymphocyte and monocytes isolated from blood samples (basal). The immune function was studied by proliferation assays. The influence of hyperglycaemia was evaluated by preincubation of mononuclear cells in a HG-containing medium. 23 D2 and 11 clinically healthy individuals were evaluated. 14 D2 were metabolically decompensated with glycosylated hemoglobin (HbA1c) > 8.5 and 9 had HbA1c < 8.5. The age ranged from 65-77 years old, with 14 males and 9 females. From the 23 patients analyzed, only 9 (39%) presented lower basal GSH content (range 10-18% of control) and an increment in ROS generation (range 29-122% of basal) after an incubation with HG. In parallel, these patients presented a decrease in lymphocyte proliferation after incubation with HG (p