Disease relevance of glycolaldehyde

• 1,2-Diaminobenzene protected against the toxicity of glycolaldehyde [1].
• Glycolaldehyde induces growth inhibition and oxidative stress in human breast cancer cells [2].
• It reacted with water at 37 degrees C and pH 7.4 (phosphate buffer) to form glycolaldehyde and several related reducing compounds; none of these products were mutagenic for Salmonella typhimurium TA1535 [3].
• Pyridoxine-requiring mutants of Escherichia coli: glycolaldehyde dehydrogenase is not coded for by the pdxB gene [4].
• Synthetic peptides representing the N-terminal (residues 1-16) and internal (residues 53-65) epitopes of toxic shock syndrome toxin-1 (TSST-1) were coupled to carrier protein, and carbonyl tags were introduced by Amadori reaction with glycolaldehyde [5].

High impact information on glycolaldehyde

• The in vivo production of glycolaldehyde and other reactive aldehydes by myeloperoxidase may thus play an important pathogenic role by generating AGE products and damaging tissues at sites of inflammation [6].
• The steady-state kinetic parameters for the GLOX oxidation of methylglyoxal, glyceraldehyde, dihydroxyacetone, glycolaldehyde, acetaldehyde, glyoxal, glyoxylic acid, and formaldehyde, were determined by using a lignin peroxidase coupled-assay at pH 4 [7].
• Methylation and hydroxyacetaldehyde treatment of low density lipoprotein prevented the uptake of low density lipoprotein [8].
• Treating cells with glycolaldehyde (GA) and glyoxal (GO) strongly inhibited ABCA1-dependent transport of cholesterol from cells to apoA-I, while methylglyoxal had little effect [9].
• In vitro studies have demonstrated that glycolaldehyde, a product of serine oxidation, reacts with proteins to form N(epsilon)-(carboxymethyl)lysine (CML), a chemically well-characterized AGE [10].

Chemical compound and disease context of glycolaldehyde

• EG has in itself a low toxicity, but is in vivo broken down to four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid [11].
• Recently we demonstrated for the first time that glyceraldehyde-derived AGEs (AGEs-2) and glycolaldehyde-derived AGEs (AGE-3) have diverse biological activities on vascular wall cells, mesangial cells, Schwann cells, malignant melanoma cells and cortical neurons [12].
• Acidosis (pH 6.8) and glycine (2 mmol/L) each blocked glyoxylate, but not glycoaldehyde toxicity, indicating differing injury pathways [13].

Biological context of glycolaldehyde

• Nonenzymatic glycosylation of matrix by glycolaldehyde or G6P significantly inhibited thymidine incorporation by mesangial cells [14].
• The former was formed from D-glyceraldehyde and pyruvate through decarboxylation of pyruvate, and the latter from glycine and glycolaldehyde [15].
• Glycolaldehyde increased the matrix advanced glycation product content as measured by specific fluorescence more than two-fold, while inhibiting bone differentiation more than 90% as measured by in vivo 45CaCl2 uptake, alkaline phosphatase levels, and histology [16].
• The hydrate of glycolaldehyde is a substrate analogue that induces the formation of cob(II)alamin and 5'-deoxyadenosine from adenosylcobalamin at the active site of dioldehydrase, and the resulting complex is inactive [17].
• Authentic hydroxyethyl was synthesized from doxorubicin by reductive alkylation with glycolaldehyde [18].

Anatomical context of glycolaldehyde

• Hydrazine compounds inhibit glycation of low-density lipoproteins and prevent the in vitro formation of model foam cells from glycolaldehyde-modified low-density lipoproteins [19].
• Treatment of demineralized bone matrix particles from 35-week-old normal Long-Evans rats with glycoaldehyde, a precursor of advanced glycation end-products, was used to assess the effects of bone-matrix glycation on the process of bone differentiation [16].
• LDL modified with glycolaldehyde and glyceraldehyde labeled with (125)I was degraded more extensively by human monocyte-derived macrophages than was (125)I-labeled native LDL [20].
• The introduction of aldehydes into antigens by glycolaldehyde, which can be produced by activated neutrophils reacting with serine, or by the oxidation of an N-linked oligosaccharide with NaIO4, enhances by several orders of magnitude their immunogenicity in mice [21].
• Retinal microvascular endothelial cells (RMECs) were treated with glycoaldehyde-modified albumin (AGE-Alb) or unmodified albumin (Alb) [22].

Associations of glycolaldehyde with other chemical compounds

• We prepared three immunochemically distinct AGE by incubating bovine serum albumin (BSA) with glucose, glyceraldehyde, or glycolaldehyde [23].
• We studied the reaction of carbonyl compounds glyoxal (GO) and glycolaldehyde (GLA) with pyridoxamine (PM), a potent post-Amadori inhibitor of AGE formation in vitro and of development of renal and retinal pathology in diabetic animals [24].
• PM also inhibited the modification of lysine residues and loss of enzymatic activity of RNase in the presence of GO and GLA and inhibited formation of the AGE/ALE N(epsilon)-(carboxymethyl)lysine during reaction of GO and GLA with bovine serum albumin [24].
• In the course of investigating the chemistry of phosphonoacetaldehyde (PAL), an analogue of glycolaldehyde phosphate, we have observed a striking case of catalysis by the layered hydroxide mineral hydrotalcite ([Mg2Al(OH)6][Cl.nH2O]) [25].
• The reaction of 3-hydroxymorpholine in aqueous solution, 25 degrees C, pH 6.6, yields (2-hydroxy-ethoxy)acetaldehyde (62%), acetaldehyde (26%), and glycolaldehyde (26%), based on analysis of the dintrophenylhydrazine derivatives [26].

Gene context of glycolaldehyde

• Using breast cancer cells, we demonstrate that glycolaldehyde inactivates glucose-6-phosphate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, and Cu,Zn superoxide dismutase, suppresses cell growth, and induces apoptosis [27].
• Glycolaldehyde-modified bovine serum albumin downregulates leptin expression in mouse adipocytes via a CD36-mediated pathway [28].
• Glycolaldehyde, a reactive intermediate for advanced glycation end products, plays an important role in the generation of an active ligand for the macrophage scavenger receptor [29].
• No free glycolaldehyde (a product of xylulose 5-phosphate splitting in the transketolase reaction) was revealed [30].
• The aldA gene encodes functional ALDH and can use glycolaldehyde and glyceraldehydes as substrates [31].

Analytical, diagnostic and therapeutic context of glycolaldehyde

• The ligation state of hemoglobin during its cross-linking by glycolaldehyde influences the ultimate oxygen affinity of the cross-linked protein [32].
• The elution rate of mononuclear blood cells after treatment with ionizing radiation (600 cGy) was reduced more than 5-fold if cells were incubated with 10 mM glycolaldehyde for 2 h [33].
• METHODS: Glycolaldehyde was used to modify bovine serum albumin and HPLC analysis was used to measure pentosidine formation as an indicator of AGE formation [34].
• The paper described modified hemoglobin (Hb) with glycolaldehyde for the efficacy on resuscitation of severe hemorrhagic shock [35].

References