Erythrocyte plasma membrane redox system in first degree relatives of type 2 diabetic patients

Diabetes mellitus [TDM] is strongly associated with oxidative stress. Human erythrocytes contain a plasma membrane redox system [PMRS] which transfers electrons from intracellular donors [NADH, ascorbate] to extracellular acceptors outside the cell. We show that the activity of erythrocyte PMRS and APR reductase becomes elevated in first degree relatives of type 2 diabetics and in TDM subjects. The increase in PMRS and APR reductase signifies compensatory mechanisms to mitigate increased oxidative stress. These findings show that an impaired redox balance may be a cause the disturbance of homeostasis in type 2 diabetic families, even before the development of the disease

Oxidative stress in first degree relatives of type 2 diabetic patients

Epidemiological studies on twins and families have provided a strong correlation for genetic factors contributing to etiology of type 2 diabetes mellitus [T2DM]. Diabetes mellitus is strongly associated with oxidative stress, which can be a consequence of either increased production of free radicals, reduced antioxidant defense or both. The present work was undertaken to study known markers of erythrocyte oxidative stress: malondialdehyde [MDA] and reduced glutathione [GSH] in first degree relatives of T2DM patients, and plasma antioxidant status in an effort to understand the role of oxidative stress in the etiology of type 2 diabetes. Our results show that the antioxidant potential of the plasma is 14% lower in first degree relatives, the intracellular GSH is lower by 9% and lipid peroxidation measured in terms of MDA is elevated by 20%, compared to normal controls. These findings show that an impaired redox balance may be a cause for disturbance of homeostasis in type 2 diabetic families even before the development of the disease. We hypothesize that that oxidative stress precedes the development of overt diabetic state