Drug therapy of neuropathic pain: current developments and future perspectives.
Patiāla, India. In Curr Drug Targets, Feb 2014
The review also gives an insight into various pharmacological agents with potential neuropathic pain attenuating properties in experimental models that include NSAIDs, corticosteroids, ion channel blockers (Ca(2+), Na(+), K(+), and TRP channel); ion exchange modulators (NCE and NHE); ion/molecule transport modulators (NKCC-1 and glycine); receptor modulators (kinin, histamine, 5-HT1A, dopamine, alpha & beta adrenergic, purinergic, excitatory amino acid, sigma, ORL1, endothelin, melanocortin, ephrin and PAR); enzyme inhibitors (cytosolic kinase, metalloproteinase, protease, vasopeptidase, D-amino acid oxidase, fatty acid amide hydrolase, aldose reductase and sorbitol dehydrogenase); other ligands (AGE, RAGEs, neuropeptides, neurotrophic factor, complement cascade, cytokine, glial cell & gap junction, nitrous oxide, growth factor, cell adhesion molecule and neuronal sprouting molecule).
[The biochemical markers of hepatobiliary function in children under environmental pollution].
In Wiad Lek, 2013
Among the investigated enzymes the high frequency of abnormal levels of gamma-glutamyltransferase (54.6%) alkaline phosphatase (36.1%), sorbitol dehydrogenase (28.6%) were detected in children from ecologically unfavorable districts which may indicate that these markers were helpful for the early diagnosis of environmentally triggered hepatobiliary disease.
The current state of serum biomarkers of hepatotoxicity.
United States. In Toxicology, 2008
In contrast, the enzymatic markers sorbitol dehydrogenase, glutamate dehydrogenase, paraxonase, malate dehydrogenase, and purine nucleoside phosphorylase are all readily measured by photometric methods and use reagents that work across preclinical species and humans and are commercially available.
Pyridine nucleotide redox abnormalities in diabetes.
Boston, United States. In Antioxid Redox Signal, 2007
Our studies suggest that cytosolic NADH reductive stress under high glucose is largely caused by increased flux of glucose through polyol (sorbitol) pathway consisting of aldose reductase and sorbitol dehydrogenase.
Sorbitol dehydrogenase: structure, function and ligand design.
Australia. In Curr Med Chem, 2004
Sorbitol dehydrogenase (SDH), a member of the medium-chain dehydrogenase/reductase protein family and the second enzyme of the polyol pathway of glucose metabolism, converts sorbitol to fructose strictly using NAD(+) as coenzyme.