Tissue specific oxidative stress profile in relation to glycaemic regulation in mice.

Background: Diabetes mellitus is a metabolic disorder characterized by hyperglycaemia resulting from uncontrolled glucose regulation. Reactive oxygen species are recognized as one link between hyperglycaemia and diabetic complications. Studies have shown that diabetes mellitus is associated with decreases in antioxidant potential and increased formation of free radicals leading to oxidative stress.

Control of hyperglycemia significantly improves oxidative stress profile of pancreatic islets.

Pancreatic islets are known to express low levels of antioxidant enzymes compared to other tissues and are therefore vulnerable to oxidative stress. Enhancing antioxidant defense mechanisms in pancreatic islets help them to cope better with oxidative stress. Persistent hyperglycemia under diabetic condition leads to continuous generation of reactive oxygen species, and different tissues exposed to this are oxidatively damaged depending on their antioxidant defense.

Pancreatic islets are very poor in rectifying oxidative DNA damage.

Objective: Free radicals that escape scavenging by antioxidant defense damage lipids, proteins, and DNA. Damage to DNA can be repaired. Therefore, both cells' antioxidant defense and their ability to repair oxidatively damaged DNA decide its fate to survive oxidative stress.

Differential susceptibility of chick and mouse islets to streptozotocin and its co-relation with islet antioxidant status.

Species differences in susceptibility of islets to STZ in different mammals have been well documented. Likewise, failure of diabetes induction in birds by streptozotocin has been reported. We hypothesized that the susceptibility of islets to STZ treatment may be related to generation of reactive oxygen species (ROS) and their antioxidant defense mechanisms.