It is of great significance to use biosynthesis to transform the inorganic substance formaldehyde into organic sugars. Most important in this process was to find a suitable catalyst combination to achieve the dimerization of formaldehyde. In a recent report, an engineered glycolaldehyde synthase was reported to catalyze this reaction. It could be combined with engineered D-fructose-6-phosphate aldolase, a "one-pot enzyme" method, to synthesize L-xylose using formaldehyde and the conversion rate could reach up to 64%. This process also provides a reference for the synthesis of other sugars. With the increasing consumption of non-renewable resources, it was of great significance to convert formaldehyde into sugar by biosynthesis.
Biocatalysis ; Formaldehyde ; chemistry ; Fructose-Bisphosphate Aldolase ; metabolism ; Xylose ; chemical synthesis

Biomarkers, Tumor ; metabolism ; Formaldehyde ; Humans ; Neoplasms ; metabolism ; Paraffin Embedding ; RNA, Messenger ; metabolism ; Tissue Fixation

Formaldehyde is a compound which is believed to have had a role in evolutionary processes. On the other hand, the (methyl)glyoxalase pathway is a route being present in all biological organisms whereas its function has not yet been recognized in the biochemical machinery. In this article it is raised that (methyl)glyoxalase path might have functioned as a bridge between formose and archaic reductive citric acid cycles in surface metabolists at the early stage of evolution. According to the theory, formaldehyde was essential for the mentioned system as a raw molecule. Based on thermodynamic calculations a simple way of regulation is also shown. The simplicity of the theory may be in a good agreement with and an explanation of why the (methyl)glyoxalase system is of ubiquitous nature.
Citric Acid Cycle ; Evolution, Chemical* ; Formaldehyde/metabolism* ; Lactoylglutathione Lyase/metabolism* ; Thermodynamics

The injury of exogenous formaldehyde and its merchanism have attracted wide attention from researchers. The latest study found that mammals have a whole system for generating and clearning formaldehyde. However, the imbalance on the system for generating and clearning formaldehyde for various reasons will cause abnormal accumulation of endogenous formaldehyde in vivo, which is closely related to learning diability and memory dysfunction. The increase in endogenous formaldehyde concentration may be one of factors inducing such neurodegenerative diseases as Alzheimer's disease. The study on the relationship between endogenous formaldehyde and such neurodegenerative diseases as Alzheimer's disease is of great significance and can provide new thoughts for preventing and treating Alzheimer's disease with traditional Chinese medicines.
Alzheimer Disease ; drug therapy ; metabolism ; pathology ; Animals ; Drugs, Chinese Herbal ; therapeutic use ; Formaldehyde ; metabolism ; Humans

Formaldehyde (FA) is a ubiquitous toxic organic compound, and it has been regarded as a leukemogen. However, the mechanisms by which FA induces bone marrow toxicity remain unclear. The present study was aimed to examine the bone marrow toxicity caused by FA and the mechanism involving the expression changes of peroxiredoxin3 (Prx3) in this process. The mice were divided into four groups with 6 mice per group. Animals in the control group were exposed to ambient air and those in the FA groups to different concentrations of FA (20, 40, 80 mg/m(3)) for 15 days in the separate inhalation chambers, 2 h a day. At the end of the 15-day experimental period, all mice were killed. Bone marrow cells were obtained. The level of hydrogen peroxide (H2O2), the apoptosis rate, and the activities and protein expression levels of caspase-3 and caspase-9 were determined by biochemical assay, flow cytometry and immunohistochemistry, respectively; DNA damage and Prx3 expression levels were measured by single cell gel eletrophoresis immunohistochemistry and Western blotting, respectively. The results showed that the H2O2 level and cell apoptosis rate were significantly increased in FA groups relative to the control group. Caspase-3 and caspase-9 activities and their protein expression levels were markedly increased as well. Additionally, FA also increased the rate of DNA damage and the expression level of Prx3 compared with control group. Our study suggested that a certain concentration of FA causes the bone marrow toxicity by regulating the expression of Prx3.
Animals ; Blotting, Western ; Bone Marrow ; drug effects ; metabolism ; Formaldehyde ; pharmacology ; Homeodomain Proteins ; metabolism ; Male ; Mice

OBJECTIVETo investigate the protective role of inducible heat shock protein 70 (Hsp70) against damage induced by formaldehyde.

METHODSHuman bronchial epithelium (HBE) cells were transfected with plasmid harboring hsp70 gene to increase the protein expression level. HBE cells transfected with pcDNA3.1 plasmid were used as transfection control and HBE cells cultured at normal condition served as control. Three groups were marked as HBE/hsp70, HBE/pcDNA and HBE. Hsp70 expression levels of 3 groups were detected. The cells of HBE/hsp70 and HBE groups were exposed to different concentrations of formaldehyde (0,0.39,1.56,6.25 mmol/L) for 4 h. The contents of GSH and MDA were measured, and KCl-SDS method was applied to measure DNA-protein crosslink (DPC).

RESULTSHsp70 level in HBE/hsp70 group increased by 80% compared with HBE group. GSH contents in HBE/hsp70 group significantly increased and were 141.0, 119.6 mg/gpro at 0.39, 1.56 mmol/L, respectively (P<0.01), as compared with HBE group. However, it decreased when formaldehyde concentration increased to 6.25 mmol/L. While GSH content in HBE group remained decreasing. MDA contents in HBE/hsp70 and HBE group increased with formaldehyde. MDA content in HBE/hsp70 was 0.088 micromol/gpro and significantly lower than that (0.138 micromol/gpro) in HBE group (P<0.05) when formaldehyde concentration was 1.56 mmol/L, At the formaldehyde dose of 6.25 mmol/L MDA content in HBE/hsp70 was 0.140 micromol/gpro which was significantly lower than that (0.289 micromol/gpro) in HBE group (P<0.01). DPC% in two groups increased with formaldehyde. At the formaldehyde dose of 0.39 mmol/L, DPC% in HBE/hsp70 group was 3.94% which was significantly lower than that (6.25%) in HBE group (P< 0.01). At the formaldehyde dose of 1.56 mmol/L, DPC% in HBE/hsp70 group was 11.86% which was significantly lower than that (20.89%) in HBE group (P<0.05).

CONCLUSIONHsp70 can reduce formaldehyde-induced damages in human bronchial epithelium cells in vitro.

Cells, Cultured ; Epithelial Cells ; drug effects ; metabolism ; Formaldehyde ; toxicity ; Glutathione ; metabolism ; HSP70 Heat-Shock Proteins ; metabolism ; Humans ; Malondialdehyde ; metabolism ; Transfection

PURPOSE: E2F-1 is a transcriptor that converts G1 to S in the cell cycle, and Topoisomerase II-alpha is a key enzyme in the metabolism of DNA, and an indicator of cell replication. The purpose of this study was to evaluate the clinical validity of E2F-1 and Topoisomerase II-alpha as prognostic factors in colorectal cancer. METHODS: The expressions of E2F-1 and Topoisomerase II-alpha were studied immunohistochemically using tumor specimen sections fixed with formalin and paraffin-embedded for 84 cases of colorectal cancer. The correlation between E2F-1 and Topoisomerase II-alpha expressions, and their relationship with the clinicopathological factors, such as tumor differentiation, tumor invasion, lymph node metastasis and tumor stage were investigated. RESULTS: Of the 84 specimens, 43 (51.2%) were immunohistochemically negative for E2F-1, and 41 (48.8%) were positive. The expression of E2F-1 correlated with poor tumor differentiation, increased lymph node metastasis and high tumor stage. The expression of Topoisomerase II-alpha also correlated with poor tumor differentiation, increased lymph node metastasis and high tumor stage. The E2F-1 and Topoisomerase II-alpha expressions indices were significantly correlated. CONCLUSION: These results suggest that the expressions of E2F-1 and DNA Topoisomerase II-alpha may play a role as a prognostic factor for colorectal cancer, but further studies will be required for its comfirmation.
Cell Cycle ; Colorectal Neoplasms* ; DNA ; DNA Topoisomerases, Type I* ; Formaldehyde ; Lymph Nodes ; Metabolism ; Neoplasm Metastasis

OBJECTIVETo investigate whether formalin inflammatory pain can induce the change in heme oxygenase-1 (HO-1) expression in the spinal cord of rats or not and the time course character.

METHODS42 SD rats were divided into 7 groups (n = 6): control formalin 6 h, formalin 12 h, formalin 1 d, formalin 2 d, formalin 3 d and formalin 7 d groups. Rats were subcutaneously injected with 0.2 ml 0.5% formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The immunohistochemistry was used to observe the expression of HO-1 protein in laminae I - II of the spinal cord dorsal horn and the area around canalis centralis of the I5 spinal segment of rats.

RESULTSThere are rare HO-1 immunoreactive cells in the laminae I - II of the dorsal horn and the area around canalis centralis of the I5 spinal segment of rats of control group and HO-1 immunoreactive cells were light in staining degree. Comparing with control group, the numbers of HO-1 immunoreactive cells in the I - II laminae of dorsal horn and area around canalis centralis were increased in the rats at 6 h after formalin injection. The number and staining degree of HO-1 immunoreactive cells were further increased at 12 h and peaked at 1 d after formalin injection. They didn't return to normal level at the 7th day. There were no difference in right and left dorsal horn in the number and staining degree of HO-1 immunoreactive cells at the same time after formalin injection.

CONCLUSIONFormalin inflammatory pain induced increased expression of HO-1 in the spinal cord dorsal horn and the area around canalis centralis of rats. At 1 d after injection of formalin, the increased expression of HO-1 was the most obviously.

Animals ; Formaldehyde ; adverse effects ; Heme Oxygenase (Decyclizing) ; metabolism ; Male ; Pain ; metabolism ; Pain Measurement ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

Here we report a systematic method for constructing a large scale kinetic metabolic model and its initial application to the modeling of central metabolism of Methylobacterium extorquens AM1, a methylotrophic and environmental important bacterium. Its central metabolic network includes formaldehyde metabolism, serine cycle, citric acid cycle, pentose phosphate pathway, gluconeogensis, PHB synthesis and acetyl-CoA conversion pathway, respiration and energy metabolism. Through a systematic and consistent procedure of finding a set of parameters in the physiological range we overcome an outstanding difficulty in large scale kinetic modeling: the requirement for a massive number of enzymatic reaction parameters. We are able to construct the kinetic model based on general biological considerations and incomplete experimental kinetic parameters. Our method consists of the following major steps: (1) using a generic enzymatic rate equation to reduce the number of enzymatic parameters to a minimum set while still preserving their characteristics; (2) using a set of steady state fluxes and metabolite concentrations in the physiological range as the expected output steady state fluxes and metabolite concentrations for the kinetic model to restrict the parametric space of enzymatic reactions; (3) choosing enzyme constants K's and K'(eqS) optimized for reactions under physiological concentrations, if their experimental values are unknown; (4) for models which do not cover the entire metabolic network of the organisms, designing a dynamical exchange for the coupling between the metabolism represented in the model and the rest not included.
Citric Acid ; metabolism ; Computer Simulation ; Energy Metabolism ; Formaldehyde ; metabolism ; Kinetics ; Metabolic Networks and Pathways ; Methylobacterium extorquens ; genetics ; growth & development ; metabolism ; Models, Biological ; Serine ; metabolism ; Systems Biology ; methods

OBJECTIVETo investigate the effect of formaldehyde exposure on the expression of inflammatory cytokines in human bronchial epithelial cells (16HBE cells).

METHODS16HBE cells were treated with formaldehyde with a concentration of 0, 0.04, 0.08, 0.16, 0.32, or 0.64 mmol/L for 24 hours, and MTT assay was applied to measure proliferative activity and calculate median lethal dose; 16HBE cells were exposed to formaldehyde with a concentration of 0, 0.04, 0.16, 0.64, or 1.20 mmol/L for 4 hours, MTT assay was applied to measure proliferative activity, and enzyme-linked immunosorbent assay was applied to measure the levels of Th1, Th2, and Th17 cytokines and tumor necrosis factor α(TNF-α) in cell supernatant.

RESULTSCompared with the control group, the 0.32-and 0.64-mmol/L exposure groups had significant decreases in cell viability (P<0.05); all exposure groups had reductions in interleukin(IL)-2 and IL-12, but no significant changes in interferon-γ and IL-10. In the 1.20-mmol/L exposure group, there was an increase in IL-4, with the increasing exposure dose, IL-5 and IL-6 tended to increase first and then decrease, and there was no significant change in IL-13; with the increasing exposure dose, IL-8 tended to increase first and then decrease, and there was no significant change in IL-17. In all the exposure groups, TNF-α increased and tended to increase significantly with the increasing exposure dose(P<0.05).

CONCLUSIONFormaldehyde exposure can cause imbalance between Th1 and Th2 cytokines secreted by 16HBE cells, as well as increased expression of IL-8 and TNF-α.

Cells, Cultured ; Cytokines ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; Formaldehyde ; adverse effects ; Humans ; Interferon-gamma ; metabolism ; Interleukins ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism