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Metabolic Laboratory Data
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
The practice of Metabolic Medicine can be thought of as applied biochemistry. So, we must be astute at using the data we accumulate from lab results. The fundamentals of our field go back to what we understand about the basic cellular processes of energy and protein metabolism. We use this framework to project our imagination into what we think is happening within the patient’s body. To a very real extent, we are thinking at a cellular level when we see our patients at the bedside. Like a watchmaker peering into the gears and rotors of a fine chronograph, we use lab data to inform us on how the patient’s metabolic machinery is functioning.
Antitubulin Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Microtubules are highly dynamic cytoskeletal polymers found in all eukaryotic cells. They serve as an essential structural component within the cell and are important for the maintenance of cell shape and polarization (Figure 4.2). They are involved in a number of cellular processes including cytokinesis, mitosis, cell motility, intracellular transport, secretion, and vesicular transport.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
The daughter cells, produced after cell division, will now have the correct genetic information for controlling cellular processes. There are two forms of cell division: mitosis and meiosis. Mitosis produces two daughter cells and enables cells to replicate for growth and repair. Meiosis produces four daughter cells, each with half the number of chromosomes: haploid cells, which are important for making gametes, which fuse during fertilisation to make diploid cells, and ultimately a foetus.
How metabolism and metabolites shape immunity during disease
Published in International Reviews of Immunology, 2022
Cellular metabolism is a complex biological process governed by numerous biochemical reactions that maintain various cellular processes essential for cell survival and continuity of life. It is not only important for the maintenance of host physiology, but also plays a crucial role in shaping the host’s defense system. The dynamicity of various immune components, immune responses and immune homeostasis during steady state or infection depends on the metabolic state of immune cells. Recently, it has been shown that various metabolite and metabolic enzymes play a pivotal role in the development of host immunity. This issue of International Reviews of Immunology focuses on the amino acid, sugar and lipid metabolisms and metabolic enzymes involved in host immunity during microbial infection and in different noninfectious defenses such as cancer, metabolic diseases and autoimmune diseases (Figure 1).
Securinine Induces Differentiation of Human Promyelocytic Leukemic HL-60 Cells through JNK-Mediated Signaling Pathway
Published in Nutrition and Cancer, 2022
Jeetesh Sharma, Ankita Pandey, Sapna Sharma, Aparna Dixit
Like other cellular processes, hematopoietic stem cell differentiation is also strictly regulated by a complex network of transcription factors that function in a well-defined hierarchical set-up (48). The progenitors follow a specific expression scheme of transcription factors in order to commit to a particular lineage. The constant cross-talk among transcription factors guide precursor cells to follow the differentiation pathway. In the present study, securinine treatment resulted in a significant upregulation of PU.1 when compared to vehicle-treated cells. This is consistent with the known role of PU.1, which is recognized to be critical for both early and late stages of myeloid cells and B-lymphocytes and is markedly increased during differentiation of hematopoietic stem cells to mature myeloid and B-lymphoid cells (48). PU.1 knock out mice die due to a lack of mature myeloid and B-lymphoid cells (49). C/EBP-α and C/EBP-ε act downstream of PU.1 and regulate granulocytic differentiation. C/EBP-₂ deficient mice lack neutrophils and eosinophils but retain monocytes, lymphocytes, erythroid cells, and immature myeloblasts (50). Evidenced by the expression of monocyte surface marker, securinine treatment resulted in the differentiation of HL-60 cells toward monocytic lineages. In line with the earlier reports, we also observed significant downregulation of both C/EBP-α, C/EBP-ε genes at 96 h post-securinine treatment.
Crotonaldehyde exposure induces liver dysfunction and mitochondrial energy metabolism disorder in rats
Published in Toxicology Mechanisms and Methods, 2021
Shuman Zhang, Biao Zhang, Qi Zhang, Zhihu Zhang
Crotonaldehyde induces cytotoxicity by inducing glutathione (GSH) depletion, increasing the levels of reactive oxygen species (ROS) in the cell, and activating caspase-cascade pathway-dependent apoptosis leading to cell death (Yang et al. 2013). In addition, the decrease in intracellular ATP activity induced by crotonaldehyde also explains the transition from apoptosis to necrosis in some cells (Liu et al. 2010a). Most energy in the body is produced by the mitochondria via the electron-transport chain (ETC) and oxidative phosphorylation (OXPHOS). Cellular processes can access the energy stored in ATP molecules (Bullon et al. 2014). The ETC is composed of five complexes namely NADH dehydrogenase (complex I; C I), succinate-ubiquinone oxidoreductase (complex II; C II), ubiquinone-cytochrome c reductase (complex III; C III), cytochrome c oxidase (complex IV; C IV), and ATP synthase (complex Ⅴ; C Ⅴ) (Cogliati et al. 2018). C I–C IV use ubiquinone and cytochrome c as electron carriers, combining electron transfer with a proton pump. The proton gradient generated in this process is used to drive C V to synthesize ATP (Duchen 2004). ETC damage can inhibit ATP production, thereby disturbing mitochondrial energy metabolism, which ultimately induces liver damage (Xu et al. 2017). The integrity of mitochondrial function is the foundation of cellular life; hence, disturbance leads to destruction of cell function, which deteriorates the health of the body. Therefore, we speculate that crotonaldehyde-induced liver injury results from mitochondrial energy metabolism disruption.