Disease relevance of glyceraldehyde

• Galanin was also found to abolish glyceraldehyde-stimulated immunoreactive insulin release from the insulinoma cells [1].
• Urine glyceraldehyde excretion is elevated in the renal Fanconi syndrome [2].
• The formation of lactoyl thioester most likely occurs by the phosphate-catalyzed dehydration of glyceraldehyde to give pyruvaldehyde, which combines with thiol to form a hemithioacetal that rearranges to the thioester [3].
• Among the different types of AGE, glyceraldehyde- and glycolaldehyde-derived AGE significantly stimulated the growth and migration of human melanoma cells [4].
• In addition, they are expected to be present in selected biological conditions, such as on consumption of a high fructose diet, and syndromes associated with high glyceraldehyde excretion, such as Fanconi Syndrome, fructose-1,6-diphosphatase deficiency and tyrosinaemia [5].

Psychiatry related information on glyceraldehyde

• Glyceraldehyde-derived advanced glycation end products in Alzheimer's disease [6].
• Are the concentrations of glyceraldehyde-derived AGEs in serum or CSF elevated early in the course of dementia [7]?

High impact information on glyceraldehyde

• In the clone of RINm5F cells, whose junctional coupling and D-glyceraldehyde-induced stimulation of insulin release by aggregated cells were also inhibited by heptanol, this alkanol did not perturb intracellular pH and Ca2+ and the most distal steps of the secretion pathway [8].
• Effects of glyceraldehyde on the structural and functional properties of sickle erythrocytes [9].
• The activated form of aldose reductase exhibited monophasic kinetics with both glyceraldehyde and glucose (Km of glucose = 0.68 mM and Km of glyceraldehyde = 0.096 mM), whereas the native (unactivated) enzyme exhibited biphasic kinetics (Km of glucose = 9.0 and 0.9 mM and Km of glyceraldehyde = 1.1 and 0.14 mM) [10].
• DL-Glyceraldehyde inhibited glycolysis in HTC cells and eventually killed them [11].
• The ATP-dependent current block and reduction in anion selectivity of the Oep21 channel is relieved by the competitive binding of phosphorylated metabolic intermediates like 3-phosphoglycerate and glycerinaldehyde 3-phosphate [12].

Chemical compound and disease context of glyceraldehyde

• Serum levels of glyceraldehyde and lactate were no greater in individuals with the Fanconi syndrome than in the normals [2].
• The latter effect was mimicked by D-glyceraldehyde, 2-ketoisocaproate, anoxia and KCN; it failed to be reproduced by L-glucose or D-fructose, was unaffected by theophylline, and was inhibited by D-mannoheptulose, iodoacetate, menadione, cytochalasin B and the absence of extracellular Ca2+ [13].

Biological context of glyceraldehyde

• The limited number of sites reactive with glyceraldehyde indicate some type of selectivity in the reaction of sugar aldehydes with hemoglobin [14].
• Phosphopeptide mapping indicated that the site of phosphorylation on myosin heavy chain was the same for both KCl- and glyceraldehyde-stimulated cells [15].
• D-Glyceraldehyde causes production of intracellular peroxide in pancreatic islets, oxidative stress, and defective beta cell function via non-mitochondrial pathways [16].
• Islets of all three genotypes exhibited biphasic insulin release in response to 10 mM D-glyceraldehyde; however, overall insulin release in both heterozygotes and diabetics remained diminished as compared with the response of normal controls [17].
• The reaction of glyceraldehyde (aldotriose) with hemoglobin A is analogous to the nonenzymic glycosylation of the protein with glucose in that the initial reversible Schiff base adduct (aldimine) of aldotriose undergoes Amadori rearrangement as does that of aldohexose to form the more stable ketoamine adduct [18].

Anatomical context of glyceraldehyde

• DL-Glyceraldehyde (15 mM) evoked a rapid redistribution of PKC from the cytosol to the membrane fraction; insulin release increased concomitantly [19].
• Gestational hyperglycaemia and insulin release by the fetal rat pancreas in vitro: effect of amino acids and glyceraldehyde [20].
• However, the higher concentration of D-glyceraldehyde (5 mmol/l) suppressed D cell ssecretion in the diabetic animals at 0 and 8.3 mmol/l glucose [21].
• These findings demonstrate that while the aging process leads to a profound defect in glucose-stimulated insulin release from the pancreatic beta-cell, this defect is not present with every secretagogue, since the normal secretory response is restored in the presence of D-glyceraldehyde [22].
• Metabolic effects of D-glyceraldehyde in isolated hepatocytes [23].

Associations of glyceraldehyde with other chemical compounds

• Incubation of erythrocytes with increasing concentrations of glyceraldehyde resulted in only a small increase in the oxygen affinity, a moderate reduction in the Hill coefficient, a substantial increase in the minimum gelling concentration, and modification of up to two lysine residues per hemoglobin molecule [24].
• However, in addition to an increase in Vmax there was also an increase in Km for both substrate, DL-glyceraldehyde, and coenzyme, NADPH [25].
• Here we show that rabbit antibodies to MG-modified ribonuclease A identify proteins modified by the Maillard reaction of glucose, fructose, ribose, glyceraldehyde, glyoxal, ascorbate, and ascorbate oxidation products (dehydroascorbate, 2,3-diketogulonate, L-xylosone, and L-threose) in addition to those modified by MG [26].
• Competitive inhibition of esterase activity by glyceraldehyde and chloral hydrate furnished evidence that p-nitrophenyl acetate was hydrolyzed at the aldehyde binding site for dehydrogenase activity [27].
• In the same system, glucose and glyceraldehyde were similarly potent inhibitors of arginine-induced glucagon secretion [28].
• Structural studies of aldose reductase and the homologous aldehyde reductase in complex with inhibitor were carried out to explain the difference in the potency of enzyme inhibition [29].

Gene context of glyceraldehyde

• ALR2 shows normal hyperbolic kinetics with most substrates except with glyceraldehyde, which exhibits substrate activation [30].
• Glyceraldehyde-derived advanced glycation end-products preferentially induce VEGF expression and reduce GDNF expression in human astrocytes [31].
• The isoelectric pH was determined to be 5.40 for aldehyde reductase II and 8.25 for aldehyde reductase I. Substrate specificity studies show that neither aldehyde reductase I nor II uses glucose as substrate but that both are capable of reducing various other aldehydes such as pyridine 3-aldehyde, butyraldehyde and DL-glyceraldehyde [32].
• Evidence is presented for two new forms of mouse liver and kidney aldehyde reductase activity (designated AHR-3 and AHR-4) resolved using cellulose acetate electrophoresis zymogram techniques and stained by glyceraldehyde and NADPH as substrate and coenzyme, respectively [33].
• We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells) [34].

Analytical, diagnostic and therapeutic context of glyceraldehyde

• This RT/PCR method was also used to assess the level of Epo and GAPDH mRNA in microdissected nephron segments [35].
• With d-glucose, d-galactose, d/l-glyceraldehyde, and d-glucosamine serving as the model glycating carbohydrates, d-glucosamine was found to exhibit the greatest effect on the stability and structure of the oligonucleotide duplexes, a finding that was confirmed by circular dichroism [36].
• It is unclear how Glu/Pi interferes with cleavage, but a metabolic explanation is likely because (i) metabolic inhibitors L-glyceraldehyde, iodoacetate and cystamine exacerbated the effect and (ii) the organization of active mitochondria observed with Rhodamine 123 and confocal microscopy is disturbed by Glu/Pi [37].
• In order to define the ability of bovine lens aldose reductase (ALR2) to generate polyols from aldoses, the quantitative determination of glycerol in the presence of glyceraldehyde was performed by gas chromatography after derivatization with trifluoroacetic anhydride [38].
• During perfusions of tumors transplanted under the kidney capsule, the carbohydrates glucose and D-glyceraldehyde increased insulin secretion [39].

References