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Garcinia indica (Kokum) and Ilex aquifolium (European Holly)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Dicson Sheeja Malar, Mani Iyer Prasanth, Tewin Tencomnao, James Michael Brimson, Anchalee Prasansuklab
Garcinol treatment significantly inhibited the growth and proliferation and colony formation of oral squamous cell carcinoma cells with a concomitant induction of apoptosis and cell cycle arrest. It exerts anti-proliferative, pro-apoptotic, cell-cycle regulatory, and anti-angiogenic effects by reducing the expression of STAT-3, c-Src, JAK1, and JAK2, NK-κB, and COX-2 besides inhibiting VEGF expression (Aggarwal and Das, 2016). Inhibition of NK-κB by garcinol was mediated through the suppression of TGF-β activated kinase 1 (TAK1) and inhibitor of IkB kinase (IKK) activation (Li et al., 2013a). Further, garcinol also targets cancer cell energy producing pathway mitochondrial respiration by inhibiting ATP production, maximal respiration, spare respiration capacity, and basal respiration. Garcinol treatment reflexively boosted glycolysis apart from the upregulation of glucose transporter 1 and 4, and HIF-1α, AKT, and PTEN (Zhang et al., 2019a).
Adenine Dinucleotide
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Richard F. Mestayer, Hyla Cass
Figure 14.1 shows what we know of the many functions that NAD+ performs in healthy cells. NAD+ is essential in cell energy production—without which cells cannot do their work. It is involved in DNA repair and gene expression—the process by which genes are turned on and off. It is included in cell signaling, immune function, and the production of vital enzymes. It probably is involved in increasing the length of telomeres, which has anti-aging benefits. NAD+ is also thought to be a neurotransmitter. Any one of these functions would make NAD+ necessary, but the fact that NAD+ is involved in so many of them highlights the significance of this molecule and shows that prolonged depleted NAD+ levels can have profound health consequences. By the same token, as many of these functions consume NAD+, it is easy to see how, with accumulating stress, age, illness, and other factors, NAD+ levels can become depleted. Just how the body prioritizes which NAD+ functions it will carry out if levels are insufficient for them all is a fertile area for additional research.
Inflammation
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The primary effect of injury on the cell is the alteration of the normal relationship between cell membrane activities and cell energy metabolism. In mammalian cells, the cellular volume and electrolyte composition are regulated by the activity of membrane bound ATP-ases, usually regarded as membrane electrolyte pumps. These counteract with a tendency to reach equilibrium associated with the presence of negatively charged, nondiffusible macromolecules, predominantly proteins, which exist in both sides of the membrane.337 If the membrane pump is impaired, the cellular electrolyte and water contents are increased to be equilibrated in both sides of the membrane.385
‘Mito-Bomb’: a novel mitochondria-targeting nanosystem for ferroptosis-boosted sonodynamic antitumor therapy
Published in Drug Delivery, 2022
Jianxin Wang, Zhiyu Zhao, Yan Liu, Xinyu Cao, Fuxin Li, Haitao Ran, Yang Cao, Changjun Wu
Sonodynamic therapy (SDT), as a new treatment strategy for tumor treatment, has overcome the limitation of light penetration depth and has the advantages of minimally invasive, no radiation, and low cost (Lafond et al., 2019; Son et al., 2020; Jiang et al., 2022). Although the detailed mechanism of SDT is still unclear, it is evident that low-intensity ultrasound will lead to excessive reactive oxygen species (ROS) production when interacting with sonosensitizers, thus enhancing cytotoxicity (Son et al., 2020; Zhang et al., 2021b).In addition, an essential factor affecting SDT is the subcellular localization of sonosensitizers. Mitochondria, as the site of cell energy metabolism, also participate in various types of cell death, which has attracted the attention of researchers (Pathania et al., 2009; Guo et al., 2021). Previous studies have shown that destroying mitochondrial integrity can transmit apoptotic cell signals and initiate apoptosis. Mitochondria-targeting SDT resulted in more tumor cell apoptosis than SDT with nonselective subcellular distribution (Zong et al., 2016; Qu et al., 2020; Han et al., 2021). Therefore, mitochondria-targeting SDT is considered a more effective and promising treatment for apoptosis. However, due to the inherent anti-apoptotic ability of triple-negative breast cancer tumor (TNBC) cells, the overall effectiveness of various treatment methods, including SDT and the improvement of patient survival rate, are still not ideal (Sun et al., 2021; Yao et al., 2021). There is an urgent need to develop non-apoptotic therapies to disrupt the anti-apoptotic mechanisms of TNBC cells.
Oxidative stress-induced cardiomyocyte apoptosis is associated with dysregulated Akt/p53 signaling pathway
Published in Journal of Receptors and Signal Transduction, 2020
Nan Zheng, Han Li, Xi Wang, Zaixian Zhao, Dongkai Shan
To clarify the beneficial mechanism exerted by MAPK/p53 pathway on oxidative stress-treated cells, cellular energy metabolism and calcium balance were analyzed. As shown in Figure 4(A), ATP production was reduced by oxidative stress whereas p53/RNAi attenuates ATP reduction induced by oxidative stress, suggesting that ATP production was impaired by oxidative stress due to the activated MAPK/p53 signaling pathway. Besides, cell energy metabolism was measured through analyzing the content of glucose consumption and lactic acid production. As shown in Figure 4(B,C), the glucose consumption was reduced whereas lactic acid production was elevated after exposure to oxidative stress. However, p53/RNAi reversed glucose consumption and reduced lactic acid production. Besides, we also observed the calcium content in cytoplasm. As shown in Figure 4(D), compared to the control group, oxidative stress elevated the content of cytoplasmic calcium whereas this effect could be reversed by p53/RNAi. Overall, our results demonstrate that MAPK/p53 seems to regulate cell energy metabolism and calcium balance.
Personalized Nutrition in Disrupting Cancer — Proceedings From the 2017 American College of Nutrition Annual Meeting
Published in Journal of the American College of Nutrition, 2019
Taylor C. Wallace, Scott Bultman, Chris D’Adamo, Carrie R. Daniel, Justine Debelius, Emily Ho, Heather Eliassen, Dawn Lemanne, Purna Mukherjee, Thomas N. Seyfried, Qiang Tian, Linda T. Vahdat
The failure to manage cancer has been due in large part to the dogmatic belief that cancer is a constellation of genetic diseases (63). Emerging evidence, however, suggests that cancer is primarily a mitochondrial metabolic disease involving disturbances in energy production through respiration and fermentation (64). The disturbances in tumor cell energy metabolism are suggested to be linked to abnormalities in the structure and function of mitochondria that disrupt adenosine triphosphate (ATP) synthesis through oxidative phosphorylation (65, 66). If this is indeed the case, all cancers could be considered a single disease with a common pathophysiological mechanism involving dysfunction of mitochondrial oxidative phosphorylation. Continuing this theory, gene mutations observed in various cancers and all other recognized cancer hallmarks may be considered downstream effects, and not causes, of the initial disturbance of cellular energy metabolism (64, 67).