Aldose reductase, oxidative stress, and diabetic mellitus

Wai Ho Tang, Kathleen A Martin, John Hwa, Wai Ho Tang, Kathleen A Martin, John Hwa

Abstract

Diabetes mellitus (DM) is a complex metabolic disorder arising from lack of insulin production or insulin resistance (Diagnosis and classification of diabetes mellitus, 2007). DM is a leading cause of morbidity and mortality in the developed world, particularly from vascular complications such as atherothrombosis in the coronary vessels. Aldose reductase (AR; ALR2; EC 1.1.1.21), a key enzyme in the polyol pathway, catalyzes nicotinamide adenosine dinucleotide phosphate-dependent reduction of glucose to sorbitol, leading to excessive accumulation of intracellular reactive oxygen species (ROS) in various tissues of DM including the heart, vasculature, neurons, eyes, and kidneys. As an example, hyperglycemia through such polyol pathway induced oxidative stress, may have dual heart actions, on coronary blood vessel (atherothrombosis) and myocardium (heart failure) leading to severe morbidity and mortality (reviewed in Heather and Clarke, 2011). In cells cultured under high glucose conditions, many studies have demonstrated similar AR-dependent increases in ROS production, confirming AR as an important factor for the pathogenesis of many diabetic complications. Moreover, recent studies have shown that AR inhibitors may be able to prevent or delay the onset of cardiovascular complications such as ischemia/reperfusion injury, atherosclerosis, and atherothrombosis. In this review, we will focus on describing pivotal roles of AR in the pathogenesis of cardiovascular diseases as well as other diabetic complications, and the potential use of AR inhibitors as an emerging therapeutic strategy in preventing DM complications.

Keywords: aldose reductase; atherosclerosis; diabetes mellitus; oxidative stress; thrombosis.

Figures

Figure 1
Figure 1
Role of aldose reductase (AR) in hyperglycemia-induced oxidative stress. Excessive amount of glucose is shunted to the polyol pathway, where AR reduces glucose into sorbitol at the expense of NADPH. Since NADPH is essential for generation of GSH (intracellular antioxidant) from GSSG, the depletion of NADPH by the AR pathway may impair intracellular antioxidant defense. Sorbitol is then converted to fructose by SDH with the production of NADH, potentially leading to increased ROS via NADH oxidase.
Figure 2
Figure 2
Glucose flux through the polyol pathway has been associated with the pathogenesis of diabetic complications via several potential mechanisms. Intracellular accumulation of sorbitol causes osmotic stress. The end production of the polyol pathway, fructose, is converted to fructose-6-phosphate (F-6-P) by hexokinase, and is further converted to glucosamine-6-phosphate by glutamine: fructose-6-phosphate amidotransferase (GFAT). Fructose-6-phosphate may also form fructose-1,6-bisphosphate (F-1,6-P), which is converted to dihydroxyacetone phosphate (DHAP). DHAP and glyceraldehdye-3-phosphate (GA3P) are interconvertible by triosephosphate isomerase. They can lead to the formation of methylglyoxal, resulting in advanced glycation end-product. DHAP can further be converted to diacylglycerol (DAG), leading to PKC activation. The continuous conversion of glycerol-3-phosphate (G-3-P) to DHAP results in concomitant transfer of electrons from reduced cytosolic NADH to mitochondrial oxidized FAD, which can generate high mitochondrial membrane potentials and inhibition of the electron transport chain at complex III. The oxidation of NADH by NADH oxidase produces reactive oxygen species (ROS), which can attack the mitochondrial membrane.

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