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Converting Petrochemical Plastic to Biodegradable Plastic
Published in Martin Koller, The Handbook of Polyhydroxyalkanoates, 2020
Tanja Narancic, Nick Weirckx, Si Liu, Kevin E. O’Connor
In P. putida, efficient use of ethylene glycol as a sole carbon source requires the alternative Gcl pathway, involving the conversion of two glyoxylates to tartronate semialdehyde and CO2 through a glyoxylate carboligase and subsequent conversion to 2-phosphoglycerate, which is fed into the central metabolism at the level of the C3 pool [57] (see Figure 12.4). In P. putida KT2440, this pathway is not induced by ethylene glycol or its oxidation products. Instead, it is part of a larger metabolic context of purine metabolism induced by xanthine or allantoin as upstream metabolites [60]. Both activation of the Gcl pathway and streamlining of the upstream oxidation steps toward glyoxylate can be achieved by metabolic engineering [57]. The same can also be achieved by adaptive laboratory evolution [60]. Interestingly, these two approaches yielded completely different optimization strategies, with metabolic engineering focused on the overexpression of pathway-encoding genes, and laboratory evolution affecting the associated regulators and other nonintuitive targets such as a porin. The metabolism of ethylene glycol. PedE and PedH: quinoprotein ethanol dehydrogenase; PedI: aldehyde-dehydrogenase; GlcDEF: glycolate oxidase; Gcl: glyoxylate carboligase; Hyi: hydroxypyruvate isomerase; GlxR: tartronate semialdehyde reductase; Eno: enolase (phosphopyruvate hydratase); PykA and PykF: pyruvate kinase; TCA: tricarboxylic acids cycle.
Mammalian Cell Physiology
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
Besides its roles in protein synthesis and as an oxidizable energy substrate, glutamine can play other important roles in cellular metabolism, e.g., its role in purine metabolism. Raivio and Seegmiller (164) suggest that the availability of glutamine in the culture medium of normal and hypoxanthine phosphoribosyltransferase-deficient fibroblasts may be rate limiting for de novo purine synthesis in vitro. The first "committed step" in purine synthesis is the reaction of 5-phosphoribosyl-1-pyrophosphate (PRPP) with glutamine to form phosphoribosylamine, an example of a glutaminedependent amination (86). A second glutamine-dependent amination and an aspartate-dependent amination also occur for each molecule of inosinic acid formed. Aspartate then donates another amino group to inosinic acid to form adenosine monophosphate (AMP), which can then be converted to adenosine diphosphate (ADP) and eventually to adenosine triphosphate (ATP) (86). Glycine also contributes significantly to purine synthesis by contributing two carbon atoms and one nitrogen atom to each purine molecule formed. Aspartate is a major byproduct of glutamine metabolism in some cells (70, 71) and glycine can be formed from 3-phosphogly cerate, a glycolytic intermediate (Fig. 2). The contributions of glutamine, aspartate, and glycine to the purine molecule adenine are shown in Fig. 3.
Genome Editing and Gene Therapies: Complex and Expensive Drugs
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Strimvelis® developed by GlaxoSmithKline (GSK) was the first ex-vivo stem cell gene therapy to treat the very rare (occurs in about 15 patients per year in Europe) Severe Combined Immunodeficiency due to Adenosine Deaminase deficiency (ADA-SCID; see Section 10.3). ADA is a monogenic disorder of purine metabolism; Strimvelis® uses autologous CD34+ cells transduced to express adenosine deaminase (ADA) (for details see, e.g., Stirnadel-Farrant et al., 2018). Strimvelis® approved by the European Commission on 27 May 2016, should be recommended for treatment of ADA-SCID where a matched related bone marrow donor is unavailable (South et al., 2019).
In vivo effects of aflatoxin B1 and benzo[a]pyrene on the heart muscle of chicken embryos
Published in Journal of Environmental Science and Health, Part A, 2021
Nikola Knížatová, Martin Massányi, Łukasz M. Kołodziejczyk, Anton Kováčik, Katarína Tokárová, Agnieszka Greń, Łukasz J. Binkowski, Grzegorz Formicki, Marcela Capcarová, Peter Massányi, Norbert Lukáč
Uric acid and its salts are end products of purine metabolism. Serum uric acid would have a protective antioxidant activity. This action could help to reduce or counteract the processes that cause or appear as a result of heart failure. However, these protective properties would vanish in the intracellular environment or highly hydrophobic areas such as atherosclerotic plaques and adipose tissue.[14]
Six new lanthanide metal–organic frameworks as luminescent sensors for the detection of 1-N, TDGA, UA, and HA in urine
Published in Journal of Coordination Chemistry, 2019
Zi-Xin Zhu, Cui-Juan Wang, Dan Luo, Cheng Liu, Dong-Ning Liu, Yu-Mei Xiao, Shuang Chen, Yao-Yu Wang
To a certain extent, urine as the excretion of blood filtered through the kidney reflects the metabolic state of the whole body. Detecting biomarkers of urine is of great significance for the prevention and diagnosis of diseases. Chemical pollution has become more and more serious and people are at risk of exposure to toxic substances. The following urine metabolites are derived from common chemical pollution. 1-Naphthol (1-N), a metabolite of the insecticide carbaryl, is an established human biomarker used for assessing food intake and environmental exposure [17]. Thiodiglycolic acid (TDGA), the main metabolite of vinyl chloride or vinyl chloride monomer (VCM) in human urine, is taken as a sensitive biomarker in biological monitoring of VCM exposure, since there is a strong proportional correlation between the content of TDGA excreted in urine and the personal VCM exposure level [18]. VCM is an important industrial chemical chiefly used to produce the polymer polyvinyl chloride (PVC) [19]. Human exposure to VCM can cause cancer, hormonal disorders, fertility defects, diabetes, nerve damage, and immunosuppression [20]. Toluene is widely used. Toluene in the environment can enter the human body through the food chain and bioaccumulation, causing damage to the central nervous system. When the human body is exposed to toluene, the content of hippuric acid in the urine is increased. On the other hand, uric acid (2,6,8-trihydroxypurine, UA) is the final product of purine metabolism in vivo. Abnormal urine content in the urine will increase the risk of gout, nephritis, uremia, myocardial infarction, and cardiovascular disease. Therefore, it is necessary to develop new methods for detecting uric acid in urine and for measuring hyperuricuria [21]. In general, measurement of 1-N, TDGA, UA, and HA as markers of internal dose are important ways of assessing carbaryl, VCM, purine and toluene exposure. However, some conventional analytical methods, including gas chromatography (GC) [22], high-performance liquid chromatography (HPLC) [23, 24], inductively coupled plasma-atomic mass spectrometry (ICP-MS) [25], and atomic absorption spectrophotometry (AAS) [26], are often complicated, have low selectivity and are expensive. Yan Bing and his colleagues examined the above chemicals. They mixed lanthanide ions to non-luminescent MOFs, and the resulting luminescent fluorescent probes were relatively complex [27]. Therefore, a simple, rapid, sensitive, and recyclable sensor based system for the effective detection of metabolites in human urine is desirable and necessary.