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Analysis Of Volatile Organic Compounds For Cancer Diagnosis
Published in Raquel Cumeras, Xavier Correig, Volatile organic compound analysis in biomedical diagnosis applications, 2018
Abigail V. Rutter, Josep Sulé-Suso
In the metabolism of glucose by mammalian cells, energy is harnessed in the form of ATP through the oxidation of its carbon bonds, producing lactate as the end product or, upon full oxidation of glucose through oxidative phosphorylation in the mitochondria, CO2 (Liberti and Locasale, 2016). However, in tumor cells, the rate of glucose metabolism increases and lactate is produced even in the presence of oxygen and fully functioning mitochondria (aerobic glycolysis) (Liberti and Locasale, 2016). The change in the metabolism of glucose in cancer cells favoring glycolysis to oxidative phosphorylation even in the presence of oxygen is known as Warburg effect (Warburg, 1956) and is characterized by an increased glucose consumption and lactate production. The increased levels of lactate production lead to the cancer cell microenvironment and tissue to become acidic. This acidic environment permits breakage of the basement membrane and allows accessibility of cancer cells to blood vessels, which could lead to the development of metastases through blood (Gatenby and Gillies, 2004). Therefore, it could be hypothesized that these changes in cancer cells metabolism, when compared to non-malignant cells, could lead to the release of VOCs in breath linked to cancer.
Fundamentals of biology and thermodynamics
Published in Mohammad E. Khosroshahi, Applications of Biophotonics and Nanobiomaterials in Biomedical Engineering, 2017
According to Hanahan and Weinberg (2000), virtually all cancers can be characterized by the following hallmarks: (1) Self-sufficiency in growth signals, (2) Insensitivity to anti-growth signals, (3) Anti-growth signals, (4) Tissue invasion and metastases, (5) Limitless replicative potential, (6) Sustained angiogenesis, and (7) Evasion of apoptosis. From a physical point of view, additional characteristics can be considered as both common and important for cancer initiation and progression: (a) Mechanical and structural: (i) Change in viscoelasticity of cells, i.e., a higher level of rigidity of the extracellular matrix (ECM) and a lower level of rigidity of the cancer cells compared to the normal cells, (ii) Change in membrane composition, i.e., over-expression of signaling proteins or p-glycoproteins, (iii) Epithelial-to-mesenchymal transition in cell morphology and associated reduction in the cells function synchronization and higher level of motility, (iv) Elimination of various signaling pathways, particularly apoptotic, allowing cancer cells to survive, spread in foreign organs, (v) Manufacturing and secretion of specialized proteins to dissolve basement and other membranes to facilitate cell motility, (b) Metabolic: (i) Warburg effect, which results in an increased production of metabolic energy using the glycolytic rather than oxidative phosphorylation pathways, (ii) Hypoxia, which is correlated with the glycolytic switch, (iii) A decrease of the trans-membrane potential, and (iv) A reduction in the cellular pH value which is likely also related to the Warburg effect.
The ROS/NF-κB/HK2 axis is involved in the arsenic-induced Warburg effect in human L-02 hepatocytes
Published in International Journal of Environmental Health Research, 2022
Fanshuo Yin, Ying Zhang, Xin Zhang, Meichen Zhang, Zaihong Zhang, Yunyi Yin, Haili Xu, Yanmei Yang, Yanhui Gao
It has been reported that treatment with arsenic at a concentration <1.0 μmol/L for 72 h induced the proliferation of primary keratinocytes, the target cells in arsenic-induced Bowen’s disease (Lee et al. 2011; Ran et al. 2021). This suggested that abnormal cell proliferation is the initial stage of arsenic carcinogenesis. It is therefore feasible to study arsenic-induced malignant transformation using cell proliferation as the initial step in this process. The rapid proliferation of cells requires a large amount of energy and nutrients. The Warburg effect was proposed to be a characteristic of tumor cells that prefer glycolysis to generate ATP even under aerobic conditions (Warburg 1956; Shin and Koo 2021). This phenomenon indicated by increases in glucose intake and lactate accumulation can also be observed in cultured human primary cells, cell lines chronically exposed to low-dose arsenic (Luo et al. 2016), and arsenic-transformed L-02 cells (Lou et al. 2022). More importantly, the Warburg effect has been shown to be required for maximal acquisition of anchorage-independent growth in BEAS-2B cells exposed to arsenic (Wang et al. 2020a). Key enzymes of glycolysis and certain signaling pathways that regulate the Warburg effect may also be the link between arsenic and the Warburg effect (Wang et al. 2020c). It is therefore necessary to investigate the signaling pathway and genes involved in the Warburg effect induced by arsenic in order to determine the mechanism of its carcinogenesis.
Carnosine in health and disease
Published in European Journal of Sport Science, 2019
Guilherme Giannini Artioli, Craig Sale, Rebecca Louise Jones
The effects of carnosine on tumour cells seem in direct contrast to the effects on other cell types, where carnosine has been shown to increase cell viability. It has been suggested that these apparent differences can be reconciled, however, by considering the different metabolic differences between cancer cells and other cells where carnosine is seemingly pro-proliferative (Gaunitz & Hipkiss, 2012). Most cells derive their energy from oxidative phosphorylation under normoxic conditions, whereas cancer cells have a high dependence on glycolysis (known as the Warburg effect) for their ATP production, which results in the production of lactate even in the presence of sufficient oxygen (Oppermann, Schanbel, Meixensberger, & Gaunitz, 2016). It has been suggested that the primary mechanism for the anti-neoplastic effects of carnosine relates to its ability to inhibit glycolysis (Renner, Asperger, et al., 2010). Hipkiss and Gaunitz (2014) recently suggested that there are several possibilities to explain carnosine’s effects on glycolytic activity that, in turn, underpin the anti-neoplastic effects shown in cancer cells. These were reported to include effects on (a) glycolytic enzymes, (b) metabolic regulatory activities, (c) redox biology, (d) protein glycation, (e) glyoxalase activity, (f) apoptosis, (g) gene expression and (h) metastasis. Oppermann et al. (2016) provided some evidence in support of this, but also suggested that the anti-neoplastic effects of carnosine on glioblastoma cells are attenuated in the presence of higher pyruvate, which is independent of oxidative phosphorylation.
Retention of functional characteristics of glutathione-S-transferase and lactate dehydrogenase-A in fusion protein
Published in Preparative Biochemistry & Biotechnology, 2018
S. Lalitha Gavya, Neha Arora, Siddhartha Sankar Ghosh
Lactate dehydrogenase (LDH), catalyzing the final step of glycolysis, is a tetramer composed of different combinations of LDH M and LDH H subunits encoded by LDHA and LDHB genes, respectively.[17] The two subunits favor opposite reactions, with LDH M catalyzing the conversion of pyruvate to lactate with regeneration of nicotinamide adenine dinucleotide (NAD+) from nicotinamide adenine dinucleotide reduced (NADH). Muscle cells and liver, where anaerobic metabolism is common, predominantly express LDH 5 isozyme, a homotetramer of M subunits, which aids in adenosine triphosphate generation regardless of oxygen deficient conditions. Tumor cells survive hypoxic conditions by overexpressing LDH 5, thereby directing the metabolic flux from oxidative phosphorylation to increased glycolysis, a malignant characteristic called the Warburg effect.[18,19] LDH 5 replenishes NAD+ level in the cells for glycolysis to be performed incessantly and hence, cystolic NADH and LDH 5 concentrations serve as an indicator of metabolic state of cells and the rate of glycolysis under various pathophysiological conditions.[202122] In addition to energy metabolism, NAD+ and NADH are used in apoptosis, calcium homeostasis, and regulation of oxidative stress in cells.[222324] Reports have unveiled significant differences in the intracellular NADH concentration (approximately 1.8 fold) and redox ratio between nonmalignant and malignant tissues.[25262728]