Degradation Of Aldehydes Research Articles

Genetic Profile of Myeloid Neoplasms Developed with Fanconi Anemia and Aldehyde Degradation Deficiency Syndrome

Background Fanconi anemia (FA) is an inherited bone marrow failure syndrome which develops on the basis of defective cellular responses to DNA damage. Aldehyde degradation deficiency (ADD) syndrome has been recently found as a disease caused by the defect of degradation of endogenous formaldehyde, which shares similar clinical features with FA. Although genomic abnormalities in these diseases have been associated with the high propensity of myeloid malignancies such as myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), the mechanism of the early development of MDS/AML remains unclear. Therefore, in this study, we aimed to understand the mechanism of the development of hematological malignancies by analyzing the genomic abnormalities seen in these diseases. Method We performed whole-exome sequencing (WES) and whole-genome sequencing (WGS) for 2 AML and 6 MDS developed in Japanese patients with FA (n = 6) and ADD syndrome (n = 2). Skin or bone marrow fibroblasts derived from the same patients were also studied as germline controls. We investigated somatic mutations, structural variants (SVs), and copy number alterations (CNAs) by WES and WGS. Mutational signature was analyzed to understand the mutational processes in these diseases. Result The number of somatic mutations and CNAs in AML identified by WES were 24 and 5 per patient on average, respectively, which were higher than those in MDS (6.8 mutations and 1.8 CNAs per patient) (P=0.07 and 0.06, respectively). However, no significant difference was observed for the number of SVs identified by WGS between MDS (35 counts per patient) and AML (52 counts per patient). Somatic mutations affected known driver genes in myeloid malignancies, such as RUNX1 (n = 1), ASXL1 (n = 1), SRSF2 (n = 1) and NRAS (n = 1) (Figure1). SVs also involved known driver genes in myeloid malignancies, such as CBL (n = 1), KDM6A (n = 1), PHF6 (n = 1), and RUNX1 (n = 1). In total, RUNX1 was most frequently altered (2/6, 33%). CNAs were more frequently accumulated in recurrent regions, including +1q (n = 5), +3q (n = 4), and -7q (n = 2) (Figure1). As previously reported, MDM4 and EVI1 were contained in +1q and +3q, respectively. Higher cancer cell fraction implied that most of these copy number changes were clonal, which suggested the early acquisition of copy number changes and their driver role in leukemic transformation. For mutational signatures, three known signatures were identified, which included clock-like SBS1 and SBS5 caused by endogenous mutational processes, and SBS3 related to defective homologous recombination. In addition, a novel mutational signature (Sig-A) was also detected. SBS3 and Sig-A were mainly detected in patients with FA and ADD syndrome, respectively, indicating that the different mutational processes are operating in the two diseases. Conclusion WES and WGS revealed the genetic landscape of FA and ADD syndrome mutation accumulation. Myeloid neoplasms related with FA and ADD syndrome were characterized by a unique pattern of driver mutations and CNAs, such as RUNX1 mutations/SVs, +1q and +3q. Although the two diseases share some clinical features, our study has revealed the different mutational processes in these diseases. Further investigation is warranted to reveal the underling mechanisms of mutation accumulation and the role of driver mutations in these diseases.

Fanconi anemia and Aldehyde Degradation Deficiency Syndrome: Metabolism and DNA repair protect the genome and hematopoiesis from endogenous DNA damage

We have identified a set of Japanese children with hypoplastic anemia caused by combined defects in aldehyde degrading enzymes ADH5 and ALDH2. Their clinical characteristics overlap with a hereditary DNA repair disorder, Fanconi anemia. Our discovery of this disorder, termed Aldehyde Degradation Deficiency Syndrome (ADDS), reinforces the notion that endogenously generated aldehydes exert genotoxic effects; thus, the coupled actions of metabolism and DNA repair are required to maintain proper hematopoiesis and health.

Effect of long-term influx of tertiary treated wastewater on native bacterial communities in a dry valley topsoil: 16S rRNA gene-based metagenomic analysis of composition and functional profile.

Although dumping treated wastewater into soil might provide nutrients and organic matter, it can also expose the ecosystem to biological and chemical risks. A vital indication of soil health and quality is the soil microbial community. The current work used next-generation 16S rRNA gene amplicon sequencing to evaluate the effects of the long-term influx of tertiary treated wastewater (TWW) into Wadi Uranah, a dry valley in Makkah city, Saudi Arabia, on native topsoil bacterial community composition and predicted functions. The findings demonstrated that neither the compositions of microbial communities nor their predicted functions using PICRUSt2 differed significantly (p>0.05) between polluted valley soil (PolVS) and unpolluted valley soil (UPVS). Alpha and beta diversity, however, showed that the PolVS samples had a considerably higher level of diversity and variability. Firmicutes, Actinobacteria, Proteobacteria, and Bacteroidetes were the most prevalent phyla in both groups. Noticeable relative variations existed in some metabolic pathways such as cofactor, prosthetic group, electron carrier degradation, aldehyde degradation, and Entner-Doudoroff (ED) pathways. Overall, our findings suggest that because both groups have very similar core microbiomes and functions, the long-term disposal of tertiary TWW into Wadi Uranah may have little to no influence on the composition and function of soil bacterial communities. In addition, the long-term discharge of tertiary TWW after partially treated wastewater's initial disposal may have helped the native soil microbial community recover.

Antioxidant effect of yeast on lipid oxidation in salami sausage.

Salami is a kind of fermented meat product with rich nutrition and unique flavor. Because it is rich in fat, it is easy to oxidize to produce bad flavor. Compared with the way of adding artificial or natural antioxidants to reduce the degree of sausage oxidation, the antioxidant characteristics of developing the starter itself deserve more attention. In this study, firstly the antioxidant activities of 5 strains of yeast were measured in vitro, and then the mixture of yeast and Lactobacillus rhamnosus YL-1 was applied to fermented sausage model. The effect of the starter in the sausage model was investigated through physicochemical parameters, degree of fat oxidation, free fatty acid content, and though volatile flavor compound analysis, sensory evaluation and various indexes after storage were observed. Metagenomics was used to explore metabolic pathways, functional genes and key enzymes related to lipid oxidizing substances in sausage in yeast. The results showed that Wickerhamomyces anomalus Y12-3 and Y12-4 had strong tolerance to H2O2, and had higher SOD and CAT enzyme activities. The addition of yeast effectively reduced the material value of peroxidation value and active thiobarbiturate in salami. In flavor analysis, the content of flavor compounds associated with lipid oxidation, such as hexanal, heptanal, nonanal and (E)-2-decenal were significantly lower with the use of Debaryomyces hansenii Y4-1 and Y12-3. Meanwhile, the possible pathways of yeast metabolism of flavor substances related to lipid oxidation (mainly aldehydes) were discussed with the help of metagenomic techniques. According to the results of metagenomics, fatty acid degradation (ko00071) metabolic pathway was related to the degradation of aldehydes through aldehyde dehydrogenase, which was the potential key enzyme.

A new Fanconi anemia-like disorder, aldehyde degradation deficiency syndrome: two defense mechanisms working together for the genome and hematopoiesis

Fanconi anemia (FA), a hereditary bone marrow failure syndrome, has been suggested to be caused by a defect in DNA repair that removes endogenous DNA damage due to aldehydes. In seven Japanese children with aplastic anemia who clinically resembled FA, we identified biallelic variants of the ADH5 gene, encoding formaldehyde degrading enzyme, and a heterozygous ALDH2 variant (rs671). We conclude that the combined defects in ADH5/ALDH2 caused a new disorder now termed Aldehyde Degradation Deficiency Syndrome (ADDS). We suggest that this disease is caused by defective removal of formaldehyde produced by histone demethylation during hematopoietic cell differentiation. Therapeutic targeting of formaldehyde may reduce the hematopoietic deficits of FA as well as ADDS.

Multi-omics revealed the formation mechanism of flavor in salted egg yolk induced by the stages of lipid oxidation during salting

To explore the contribution of different lipid oxidation stages to flavor formation in salted egg yolk, potential pathways of flavor formation were characterized by multi-omics strategy and partial least squares structural equation model (PLS-SEM). 72 lipids, 135 metabolites and 5 volatiles related to lipid oxidation were screened out. The degradation of aldehydes and ketones, and the generation of tryptamine and elaidic acid, etc. were promoted by triglycerides (TG) (10:0 16:0 18:1), triglycerides (TG) (18:0 20:1 22:0), etc. at primary and secondary oxidation stage, respectively. The generation of acetophenone, thianaphthene, etc. through the pathway of 2-phenylacetamide, hexanoylcarnitine, etc. was facilitated by these triglycerides (TG) at primary oxidation stage. Furthermore, amino acid metabolisms, pentose phosphate pathway and linoleic acid metabolism occurred at secondary oxidation stage were key pathways to form distinctive flavor. In conclusion, secondary oxidation stage may be more important for the formation of unique flavor (taste) in salted egg yolk.

Mechanistic study on the depolymerization of typical lignin-derived oligomers catalyzed by Pd/NbOPO4

The depolymerization mechanisms of lignin-derived oligomers over Pd/NbOPO4 catalyst were investigated by Density Functional Theory (DFT) calculations. Taking the lignin-derived typical small molecular oligomer obtained from pubescens solvolysis as an example, the formation of 4-substituted syringol and 4-ethyl guaiacol products was explored on the surface of NbOPO4 (100) and Pd55 cluster. The synergistic effect of the two kinds of active phase in depolymerization of oligomer was revealed. The NbOPO4 facilitated the breakage of β-O-4 and C-O ester bond in the two dimer fragments (O-I and O-II) from oligomer, due to strong interaction between Nb and O atoms in the dimers. The energy barriers were predicted to be 0.14 eV for β-O-4 bond cleavage and 0.92 eV for C-O ester bond, respectively. The Pd catalyst promoted C-C bond cleavage and hydrogenation in the subsequent transformation. The Cα-Cβ bond breakage was the RDS in the degradation of aldehyde (Frag-2) to 4-methyl syringol. While Cβ-Cγ bond breakage was the RDS in transformation of the acid (Frag-3) and alcohol (Frag-4) fragments, with the energy barriers of 1.73 eV and 1.36 eV, respectively. Moreover, the energy barrier for the conversion of carboxyl group to aldehyde group in Frag-3 was 1.60 eV. In these processes, ethylene, aldehyde or CO2 were released, accompanied by the formation of 4-substituted syringols and 4-ethyl guaiacol products. The mechanistic insights gained from this study could provide useful information for the design of new catalyst for the depolymerization and conversion of oligomers derived from lignin.

1-MCP extends the shelf life of ready-to-eat ‘Hayward’ and ‘Qihong’ kiwifruit stored at room temperature

Near eating-stage fruit of ‘Hayward’ and ‘Qihong’ kiwifruit (firmness 20 N) were treated with 0.5 µL L −1 1-Methylcyclopropene (1-MCP) for 12 h at room temperature (23 ±1 °C), and then stored at 23 ± 1 °C for several days. Compared with control fruit, 1-MCP greatly delayed loss of firmness, and extended the room-temperature shelf life of ready-to-eat kiwifruit by an extra 8 d (‘Hayward’) or 10 d (‘Qihong’). The 1-MCP treatment also slowed the declines in titratable acidity and color, but had no significant effects on soluble solids content (p < 0.05). Although in the 1-MCP treated fruit the amounts of total volatiles increased during room-temperature storage, the concentration of total volatiles was lower in the treated fruit compared with the untreated controls. Treatment with 1-MCP inhibited ester production and aldehyde degradation. At edible firmness, kiwifruit treated with 1-MCP showed similar fruit quality compared with the untreated controls, with similar mean values in soluble solids content, titratable acidity and color (p > 0.05). 1-MCP also decreased ethylene production and respiration rate. Moreover, the activities of superoxide (SOD), catalase (CAT) and peroxidase (POD) were increased in the treated fruit compared with the controls. The results indicate treatment with 1-MCP is a potentially effective way of prolonging the room-temperature (23 ± 1 °C) shelf life of ready-to-eat kiwifruit and maintaining their eating quality under commercial conditions.

Combined adaptive evolution and transcriptomic profiles reveal aromatic aldehydes tolerance mechanisms in Yarrowia lipolytica

Yarrowia lipolytica is an efficient oleaginous yeast, whereas its activity is typically reduced by inhibitors present in lignocellulosic hydrolysate. Understanding the response mechanism of Y. lipolytica to hydrolysate inhibitors and developing inhibitor tolerant strains are vital to lignocellulose valorization by this promising species. In this study, through adaptive laboratory evolution on three representative aromatic aldehyde inhibitors, evolved strains were obtained. Fermentation phenotype suggested that aromatic aldehydes conversion was one main reason for high tolerance of adapted strains. Transcriptome profiling analysis and reverse metabolic engineering confirmed that overexpressing the aldehyde ketone reductase gene YALI0_B07117g and aldehyde dehydrogenase gene YALI0_B01298g effectively converted aromatic aldehyde to corresponding alcohols and acids. The potential degradation pathways for aromatic aldehyde inhibitors in Y. lipolytica XYL+ were then discussed. This study provided insights to the aromatic aldehyde degradation in Y. lipolytica and a reliable basis for the development of aromatic aldehyde tolerant strains.

Aldehyde degradation deficiency (ADD) syndrome: discovery of a novel fanconi anemia-like inherited BMF syndrome due to combined ADH5/ALDH2 deficiency

We have recently described the identification of a novel inherited bone marrow failure syndrome. The first set of patients was diagnosed through the exome analysis of cells from Japanese patients with hypoplastic anemia, which have been deposited to the JCRB cell bank for quite some time previously. Originally, these cases were diagnosed with a novel disorder based on increased levels of sister chromatid exchanges in lymphocytes; however, causative genes were clarified only after applying the recently developed next-generation sequencing technology. Aldehyde degradation deficiency syndrome (ADDS) is caused by combined defects in two genes, ADH5 and ALDH2, which are both critical for degrading endogenously generated formaldehyde. Formaldehyde is highly reactive and toxic to biological molecules including DNA, and its endogenous generation in the absence of the degradation system results in DNA damage that overwhelms the DNA repair capacity, leading to the development of BMF with loss of hematopoietic stem cells and progression to MDS/leukemia. In this short review, we would like to summarize what is known today about ADDS for a wide readership of hematology clinicians in Japan.

New insights into inherited bone marrow failure syndrome

Inherited bone marrow failure syndromes (IBMFS) are a heterogeneous group of genetic disorders characterized by bone marrow failure, congenital anomalies, and increased risk of malignant disease. Next generation sequencing methods have greatly facilitated the discovery of genetic etiology in IBMFS. Recently, de novo mutations activating TP53 were detected in patients with BMFS, mimicking Diamond-Blackfan anemia (DBA), using whole exome sequencing, and these patients were recognized as having a novel disorder. This discovery provides important insights into the previously postulated connection between p53 activation and IBMFS. Furthermore, a novel IBMFS, aldehyde degradation deficiency syndrome, was found in patients with aplastic anemia resembling Fanconi anemia (FA). This disorder is caused by combined inactivating mutations in ADH5 and ALDH2 coding formaldehyde-detoxifying enzymes. In this review, we highlight recent studies on DBA, FA, and their related diseases in Japan.

Aldehyde dehydrogenase-2 activation decreases acetaminophen hepatotoxicity by prevention of mitochondrial depolarization

Oxidative stress contributes to acetaminophen (APAP) hepatotoxicity. Since lipid peroxidation produces reactive aldehydes, we investigated whether activation of mitochondrial aldehyde dehydrogenase-2 (ALDH2) with Alda-1 decreases liver injury after APAP. Male C57BL/6 mice fasted overnight received Alda-1 (20 mg/kg, i.p.) or vehicle 30 min before APAP (300 mg/kg, i.p.). Blood and livers were collected 2 or 24 h after APAP. Intravital multiphoton microscopy of rhodamine 123 (Rh123) and propidium iodide (PI) fluorescence was conducted 6 h after APAP administration to detect mitochondrial polarization status and cell death. 4-Hydroxynonenal protein adducts were present in 0.1% of tissue area without APAP treatment but increased to 7% 2 h after APAP treatment, which Alda-1 blunted to 1%. Serum alanine and aspartate aminotransferases increased to 7594 and 9768 U/L at 24 h respectively, which decreased ≥72% by Alda-1. Alda-1 also decreased centrilobular necrosis at 24 h after APAP from 47% of lobular areas to 21%. N-acetyl-p-benzoquinone imine protein adduct formation and c-Jun-N-terminal kinase phosphorylation increased after APAP as expected, but Alda-1 did not alter these changes. Without APAP, no mitochondrial depolarization was detected by intravital microscopy. At 6 h after APAP, 62% of tissue area showed depolarization, which decreased to 33.5% with Alda-1. Cell death as detected by PI labeling increased from 0 to 6.8 cells per 30× field 6 h after APAP, which decreased to 0.6 cells by Alda-1. In conclusion, aldehydes are important mediators of APAP hepatotoxicity. Accelerated aldehyde degradation by ALDH2 activation with Alda-1 decreases APAP hepatotoxicity by protection against mitochondrial dysfunction.

Aldehyde dehydrogenase-2 activation by Alda-1 decreases necrosis and fibrosis after bile duct ligation in mice

Background and aimLiver fibrosis is a leading cause of mortality worldwide. Oxidative stress is a key component in the pathogenesis of liver fibrosis. We investigated the role of aldehyde formation resulting from lipid peroxidation in cholestatic liver injury and fibrosis. MethodsC57Bl/6J mice underwent bile duct ligation (BDL) or sham operation. One hour after surgery and daily thereafter, animals were given Alda-1 (20 mg/kg, s.c.), an aldehyde dehydrogenase-2 activator, or equivalent volume of vehicle. Blood and livers were collected after 3 and 14 days. ResultsSerum alanine aminotransferase (ALT) increased from 39.8 U/L after sham operation to 537 U/L 3 days after BDL, which Alda-1 decreased to 281 U/L. Biliary infarcts with a periportal distribution developed with an area of 7.8% at 14 days after BDL versus 0% area after sham operation. Alda-1 treatment with BDL decreased biliary infarcts to 1.9%. Fibrosis detected by picrosirius red staining increased from 1.6% area in sham to 7.3% after BDL, which decreased to 3.8% with Alda-1. Alda-1 suppression of fibrosis was additionally confirmed by second harmonic generation microscopy. After BDL, collagen-I mRNA increased 12-fold compared to sham, which decreased to 6-fold after Alda-1 treatment. Smooth muscle α-actin expression in the liver, a marker of activated stellate cells, increased from 1% area in sham to 18.7% after BDL, which decreased to 5.3% with Alda-1. CD68-positive macrophages increased from 33.4 cells/field in sham to 134.5 cells/field after BDL, which decreased to 64.9 cells/field with Alda-1. Lastly, 4-hydroxynonenal adduct (4-HNE) immunofluorescence increased from 2.5% area in sham to 14.1% after BDL. Alda-1 treatment decreased 4-HNE to 2.2%. ConclusionAccelerated aldehyde degradation by Alda-1 decreases BDL-induced liver necrosis, inflammation, and fibrosis, implying that aldehydes play an important role in the pathogenesis of cholestatic liver injury and fibrosis.

Formation of odorous and hazardous by-products from the chlorination of amino acids

The formation of odorous aldehydes and N-chloraldimines, and also nitriles, which are potentially hazardous to human health, was investigated in studies of the chlorination of amino acids (AAs) in both operational drinking water treatment plants and laboratory-based experiments. In the drinking water treatment plants studied, the concentration of total free AAs did not significantly change after treatment, even though good removal of DOC was observed. However, free AAs still contributed less than 3% of total nitrogen in the treated drinking waters, and no aldehydes, N-chloraldimines or nitriles of interest were detected in the treated waters, presumably due to the low concentrations of the precursor AAs in these water samples. Laboratory formation potential experiments showed that carboxylic acids can form from the degradation of aldehydes and nitriles. Volatile carboxylic acids could result in odour issues and some carboxylic acids may be of potential health concern. Therefore, carboxylic acids should also be considered as potential by-products of interest in distribution systems with long contact times of ≥ 7days. A higher proportion of nitrile formation, and promotion of carboxylic acid formation, was observed when the chlorine to AA ratio was greater than 4 compared to when this ratio was 2.8, indicating that the Cl:AA ratio is an important factor in DBP formation pathways. This suggests that results from laboratory formation studies undertaken at these low Cl:AA ratios cannot be directly applied to ‘real’ water systems, which typically have Cl:AA ratios that are orders of magnitude higher than 4. Laboratory formation potential experiments also showed that the short-term rate of formation of aldehydes and N-chloraldimines was reduced in the presence of ammonia, although formation over longer timescales (e.g. 7 days) was not significantly different between chlorination and chloramination experiments. Therefore, the use of chloramination instead of chlorination does not appear to reduce the formation of these by-products from AAs.

Innovative and stable TiO 2 supported catalytic surfaces removing aldehydes under UV-light irradiation

The present study reports the photocatalytic degradation of aldehydes using TiO2 impregnated polyester (PES) and glass fiber (GFT)-TiO2 addressing the photocatalytic degradation aldehydes (air-solid interface). The PES-TiO2 optical absorption was determined by diffuse reflectance spectroscopy (DRS). By X-ray diffraction (XRD), the formation of TiO2 anatase on the PES surface was detected. The photocatalytic oxidation (PCO) of butyraldehyde and isovaleraldehyde was carried out in a batch photo-reactor equipped with a UV-mercury Philips 9W lamp and mediated by glass fiber GFT-TiO2 and PES-TiO2 surfaces. The removal of these two aldehydes was found to be a function of pollutant concentrations. The stable catalytic reuse of both catalysts reported. A Langmuir Hinshelwood (L-H) model describes the degradation kinetics on PES-TiO2 and on GFF-TiO2. The aldehyde degradation by-products were analyzed by gas chromatography mass spectrometry (GC-MS). Three organics intermediates identified during the aldehyde degradation were: acetones, alcohols and fatty acids.

Release and Formation of Oxidation-Related Aldehydes during Wine Oxidation.

Twenty-four Spanish wines were subjected to five consecutive cycles of air saturation at 25 °C. Free and bound forms of carbonyls were measured in the initial samples and after each saturation. Nonoxidized commercial wines contain important and sensory relevant amounts of oxidation-related carbonyls under the form of odorless bound forms. Models relating the contents in total aldehydes to the wine chemical composition suggest that fermentation can be a major origin for Strecker aldehydes: methional, phenylacetaldehyde, isobutyraldehyde, 2-methylbutanal, and isovaleraldehyde. Bound forms are further cleaved, releasing free aldehydes during the first steps of wine oxidation, as a consequence of equilibrium shifts caused by the depletion of SO2. At low levels of free SO2, de novo formation and aldehyde degradation are both observed. The relative importance of these phenomena depends on both the aldehyde and the wine. Models relating aldehyde formation rates to wine chemical composition suggest that amino acids are in most cases the most important precursors for de novo formation.

Lipid-derived aldehyde degradation under thermal conditions

Nucleophilic degradation produced by reactive carbonyls plays a major role in food quality and safety. Nevertheless, these reactions are complex because reactive carbonyls are usually involved in various competitive reactions. This study describes the thermal degradation of 2-alkenals (2-pentenal and 2-octenal) and 2,4-alkadienals (2,4-heptadienal and 2,4-decadienal) in an attempt to both clarify the stability of aldehydes and determine new compounds that might also play a role in nucleophile/aldehyde reactions. The obtained results showed that alkenals and alkadienals decomposed rapidly in the presence of buffer and air to produce formaldehyde, acetaldehyde, and the aldehydes corresponding to the breakage of the carboncarbon double bonds: propanal, hexanal, 2-pentenal, 2-octenal, glyoxal, and fumaraldehyde. The activation energy of double bond breakage was relatively low (∼25kJ/mol) and the yield of alkanals (10–18%) was higher than that of 2-alkenals (∼1%). All these results indicate that these reactions should be considered in order to fully understand the range of nucleophile/aldehyde adducts produced.

Facile Synthesis of Phosphate-Functionalized MWCNT-TiO2 Nanocomposites as Efficient Photocatalysts and Insights into the Roles of Nanostructured Carbon.

Effectively contacted multiwalled carbon nanotube (MWCNT)-titanium dioxide nanocomposites and phosphate-functionalized MWCNT-TiO2 composites have been successfully synthesized by simple one-pot phase-separated hydrolysis-solvothermal processes. The key to this synthetic strategy is to disperse MWCNTs uniformly in Ti(OBu)4 in advance and then to put them into the toluene organic phase. The as-prepared nanocomposites between TiO2 and the correct amount of MWCNT exhibits higher activity in the photocatalytic degradation of rhodamine B than that with the resulting TiO2 , although the activity in the photocatalytic degradation of gas-phase aldehyde and liquid-phase phenol is lower. Interestingly, the functionalization of MWCNTs with an appropriate amount of phosphoric acids prior to the synthesis could greatly improve the activity of the MWCNT-TiO2 nanocomposites for the degradation of aldehyde and phenol, even superior to that of commercial P25 TiO2 . Based on the measurements of atmosphere-controlled surface photovoltage spectra and O2 temperature-programmed desorption, it is suggested that MWCNTs are favorable to increase rhodamine B adsorption on the composite to promote the photosensitization oxidation reactions, whereas it is unfavorable for the adsorption of O2 and responsible for the low photocatalytic activity for the degradation of colorless pollutants. Phosphate functionalization greatly enhances the amount of O2 adsorbed on the MWCNT, which leads to significant charge separation, and thus, to significant photoactivity for the degradation of colored and colorless pollutants of the nanocomposites.

Plant aminoaldehyde dehydrogenases oxidize a wide range of nitrogenous heterocyclic aldehydes.

The metabolic degradation of aldehydes is catalyzed by oxidoreductases from which aldehyde dehydrogenases (EC 1.2.1) comprise nonspecific or substrate-specific enzymes. The latter subset is represented, e.g., by NAD(+)-dependent aminoaldehyde dehydrogenases (AMADHs; EC 1.2.1.19) oxidizing a group of naturally occurring ω-aminoaldehydes including polyamine oxidation products. Recombinant isoenzymes from pea (PsAMADH1 and 2) and tomato (LeAMADH1 and 2) were subjected to kinetic measurements with synthetic aldehydes containing a nitrogenous heterocycle such as pyridinecarbaldehydes and their halogenated derivatives, (pyridinylmethylamino)-aldehydes, pyridinyl propanals and aldehydes derived from purine, 7-deazapurine and pyrimidine to characterize their substrate specificity and significance of the resulting data for in vivo reactions. The enzymatic production of the corresponding carboxylic acids was analyzed by liquid chromatography coupled to electrospray ionization mass spectrometry. Although the studied AMADHs are largely homologous and supposed to have a very similar active site architecture, significant differences were observed. LeAMADH1 displayed the broadest specificity oxidizing almost all compounds followed by PsAMADH2 and 1. In contrast, LeAMADH2 accepted only a few compounds as substrates. Pyridinyl propanals were converted by all isoenzymes, usually better than pyridinecarbaldehydes and aldehydes with fused rings. The K (m) values for the best substrates were in the range of 10(-5)-10(-4)M. Nevertheless, the catalytic efficiency values (V (max)/K (m)) reached only a very small fraction of that with 3-aminopropanal (except for LeAMADH1 activity with two pyridine-derived compounds). Docking experiments using the crystal structure of PsAMADH2 were involved to discuss differences in results with position isomers or alkyl chain homologs.

Synergistic effects of high-frequency ultrasound on photocatalytic degradation of aldehydes and their intermediates using TiO 2 suspension in water

The degradation of model substances, benzaldehyde (C 6H 5CHO) and formaldehyde (HCHO), were investigated under various conditions, namely, ultrasound (US) irradiation, TiO 2 photocatalysis with UV irradiation (UV/TiO 2), and the combination of sonophotocatalysis and UV irradiation (US/UV/TiO 2), in order to clarify the synergistic effects between US and UV/TiO 2. US and UV/TiO 2 primarily contribute to the degradation of highly hydrophobic and hydrophilic substances, respectively. However, the degradation rate was found to depend on the chemical properties and concentration of not only the substances initially present, but also their decomposition intermediates. Here, the essential information for accurately evaluating the synergistic effects on reaction rate under US/UV/TiO 2 conditions is reported, with a focus on the behavior of decomposition intermediates.