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Journal ArticleDOI

Aldose and aldehyde reductases from human kidney cortex and medulla

TLDR
The results support the conclusion that there is a single human aldose reductase, and that a Aldose reducase is expressed in a reduced form, characterized by high sensitivity to aldOSE reduct enzyme inhibitors and ability to catalyze the reduction of glucose.
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This article is published in Biochimica et Biophysica Acta.The article was published on 1993-12-08. It has received 15 citations till now. The article focuses on the topics: Aldehyde Reductase & Aldose reductase.

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Citations
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Journal ArticleDOI

From hyperglycemia to diabetic kidney disease: the role of metabolic, hemodynamic, intracellular factors and growth factors/cytokines.

TL;DR: This review focuses on the metabolic factors beyond blood glucose that are involved in the pathogenesis of diabetic kidney disease, i.e., advanced glycation end-products and the aldose reductase system.
Book ChapterDOI

Polyol pathway and diabetic peripheral neuropathy

TL;DR: It is concluded that robust inhibition of metabolic flux through the polyol pathway in peripheral nerve will likely result in substantial clinical benefit in treating and preventing the currently intractable condition of diabetic peripheral neuropathy.
Journal ArticleDOI

Aldose reductase functions as a detoxification system for lipid peroxidation products in vasculitis

TL;DR: It is proposed that AR is an oxidative defense mechanism able to neutralize the toxic effects of lipid peroxidation and has a role in limiting the arterial wall injury mediated by reactive oxygen species.
Journal ArticleDOI

Substrate specificity of human aldose reductase: identification of 4-hydroxynonenal as an endogenous substrate.

TL;DR: Analysis of the binding of NADPH by fluorescence quenching techniques indicates that aldose reductase exhibits higher affinity for NADPH than NADP, suggesting that this enzyme is normally primed for reductive metabolism.
Journal ArticleDOI

Aldose Reductase and Cardiovascular Diseases, Creating Human-Like Diabetic Complications in an Experimental Model

TL;DR: The biology and pathobiology of AR actions is reviewed, suggesting that genetic ablation of AR increased atherosclerosis and increased hydroxynonenal in arteries and it was hypothesized that AR knockout prevented reduction of toxic aldehydes.
References
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Journal ArticleDOI

A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

TL;DR: This assay is very reproducible and rapid with the dye binding process virtually complete in approximately 2 min with good color stability for 1 hr with little or no interference from cations such as sodium or potassium nor from carbohydrates such as sucrose.
Journal ArticleDOI

Sorbitol, phosphoinositides, and sodium-potassium-ATPase in the pathogenesis of diabetic complications.

TL;DR: Aldose reductase inhibitors firmly link defects in myo-inositol metabolism to activation of the polyol pathway in diabetes; the resulting "sorbitol-myo- inositol hypothesis" has been extended from its application to the lenses and peripheral nerves to most of the tissues involved with diabetic complications.
Journal ArticleDOI

The aldo-keto reductase superfamily. cDNAs and deduced amino acid sequences of human aldehyde and aldose reductases.

TL;DR: Southern hybridization analysis of human genomic DNA indicates a multigene system for aldose reductase, suggesting the existence of additional proteins, and the aldo-keto reductases superfamily of proteins may have a more significant and hitherto not fully appreciated role in general cellular metabolism.
Journal ArticleDOI

Hyperglycemia, polyol metabolism, and complications of diabetes mellitus.

TL;DR: This brief review of the sorbitol pathway has attempted to present the current knowledge of this accessory pathway of glucose metabolism in the development of some diabetic complications, and the lack of knowledge of the normal role of this pathway in tissue metabolism is hampered.
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