ABSTRACT
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
Subject(s)
Humans , Adult , Oxidative Stress , NADH, NADPH Oxidoreductases , Family , Erythrocytes/enzymology , Erythrocytes/metabolism , Diabetes Mellitus, Type 2/enzymologyABSTRACT
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
Subject(s)
Humans , Diabetes Mellitus, Type 2/metabolism , Family , Malondialdehyde , Glutathione , ErythrocytesABSTRACT
Hypertension is a major problem worldwide. There is much evidence to suggest that reactive oxygen species (ROS) radical may play a role in the development of organ damage associated with cardiovascular disease and hypertension. (-)Epicatechin, a member of tea catechins belonging to flavonoid group, is known to be a potent anti-oxidant.The study has been undertaken to evaluate the effect of (-)epicatechin on markers of oxidative stress: reduced glutathione (GSH) and membrane sulfhydryl (-SH) groups in erythrocytes from hypertensive patients. The effect of (-)epicatechin was also compared with a known anti-oxidant L-ascorbic acid. The erythrocyte intracellular GSH content and membrane -SH group content were significantly (P<0.01) decreased in hypertensive subjects. In vitro incubation with (-)epicatechin caused an increase in GSH and -SH content, the effect was more pronounced in hypertensive erythrocytes. Similar results were obtained with L-ascorbic acid. The observed decrease in the level of GSH and -SH groups in hypertension is an indicator of oxidative stress condition. Observation of an increase in red cell GSH content and the protection of membrane -SH group oxidation by (-)epicatechin in hypertensive subjects is a convincing reason to suggest that high dietary intake of foods rich in catechins may help to reduce oxidative stress and concomitant free radical damage in hypertensive patients.