Oxidative-induced membrane damage in diabetes lymphocytes: effects on intracellular Ca(2 +) homeostasis

Oxidative stress is linked to several human diseases, including diabetes. However, the intracellular signal transduction pathways regulated by reactive oxygen species (ROS) remain to be established. Deleterious effects of ROS stem from interactions with various ion transport proteins such as ion channels and pumps, primarily altering Ca(2 +) homeostasis and inducing cell dysfunction. This study characterized the Ca(2 +) transport system in lymphocytes of patients with type-2 diabetes, evaluating the possible correlation between cell modifications and the existence of specific oxidative stress damage. Lymphocytes from type-2 diabetes patients displayed oxidative stress features (accumulation of some ROS species, membrane peroxidation, increase in protein carbonyls, increase in SOD and Catalase activity) and Ca(2 +) dyshomeostasis (modified voltage-dependent and inositol 1,4,5-triphosphate-mediated Ca(2 +) channel activities, decrease in Ca(2 +) pumps activity). The data support a correlation between oxidative damage and alterations in intracellular Ca(2 +) homeostasis, possibly due to modification of the ionic control in lymphocytes of type-2 diabetes patients.