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Food Interactions, Sirtuins, Genes, Homeostasis, and General Discussion
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Concerning the activity mechanism, p53 is a nuclear transcription factor with a pro-apoptotic function. Apoptosis is a natural process of programmed cell death that occurs in the body. Indeed, mutant p53 has an oncogenic potential, as more than half of the human cancers have mutated p53 (125, 128). Selective inhibition of cancer cells requires specific disruption of growth mechanisms used by these cells with limited damage to normal cells. In normal cells, the p53 protein level is low. However, when DNA is damaged by different mutagens, carcinogens, or other stress signals, this may trigger the increase of p53 protein levels, which are used to protect or repair DNA (125–129). In humans, p53 can also be damaged by different mutagens such as chemicals (pollutants, pesticides, preservatives, cigarettes, car smokes, cooking, drugs, deodorants, etc.), radiation (UV light, X rays, thermonuclear reactor, etc.), or viruses.
Cellular and Molecular Mechanisms of Ischemic Acute Renal Failure and Repair
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Joseph V. Bonventre, Ralph Witzgall
The pathological features of necrosis are very different from those of programmed cell death (Searle, et al., 1982). The latter has been called “apoptosis”, a term coined by Kerr et al., who attributes the derivation of the term to Professor James Cormack of the University of Aberdeen (Kerr, et al., 1972). “Apoptosis” is a Greek term to describe “dropping off’ or “falling off’ of petals from a flower or leaves from a tree. Pathologically, the early stages of apoptosis are characterized by disappearance of microvilli, chromatin condensation at the periphery of the nucleus, condensation of cytosolic components, breakdown of epithelial desmosomal attachments, followed by cell surface protuberances, and fragmentation of the nucleus. Ultimately there is blebbing off of cell surface protuberances containing condensed cytosol and occasional nuclear fragments, to generate spherical or ovoid “apoptotic bodies” (Wyllie, et al., 1980) which can be phagocytosed by macrophages or epithelial cells. Apoptosis histologically is often associated biochemically with cleavage of double-stranded DNA at the linker regions between nucleosomes, resulting in fragments of approximately 180 to 200 bp (Kerr and Harmon, 1991). On agarose gel electrophoresis there is a characteristic ladder pattern. The endonuclease responsible for this biochemical correlate of apoptosis has not been well characterized. A candidate enzyme is an endonuclease that is activated by calcium in thymocytes (McConkey, et al., 1988). Increases in cellular calcium concentration can induce apoptosis (Kizaki, et al., 1989).
Apoptotic Cell Death in Response to Lipopolysaccharide
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Cell death can generally proceed via necrosis or apoptosis (programmed cell death) (1–4). Necrosis is characterized by the formation of tubular lesions (pores) in the plasma membrane. On the other hand, apoptosis causes cell death in a way that differs morphologically and biochemically from necrosis. The common core mechanism of apoptosis is DNA fragmentation and morphological lesions, such as condensation and fragmentation of nucleus and cytoplasm.
Synthetic pyrethroids common metabolite 3-phenoxybenzoic acid induces caspase-3 and Bcl-2 mediated apoptosis in human hepatocyte cells
Published in Drug and Chemical Toxicology, 2022
Dilek Guvenc, Sinem Inal, Nilufer Kuruca, Sedat Gokmen, Tolga Guvenc
In mammals, there are three major types of cell death, namely, apoptosis, autophagy and necrosis (Ou et al.2017). Apoptosis means programmed cell death triggered by various physiological and pathological situations. The mechanism of apoptosis can be triggered by both intrinsic and extrinsic signaling pathways. The extrinsic pathway, known as the receptor-mediated pathway, often plays a role in inflammatory responses and cellular homeostasis (Elmore 2007). The intrinsic pathway, also known as the mitochondrial pathway, is stimulated by tetrachlorodibenzo-p-dioxin, various heavy metals, pesticides and toxins (Roy and Nicholson 2000, Curtin and Cotter 2003). Fundamental roles in the activation of this pathway are played by caspases, namely caspase-9, caspase-7, caspase-6, and caspase-3, and the Bcl-2 protein family members, including Bcl-2, Bax, Bid, Bcl-XL, especially caspase-3 and Bcl-2 proteins. The Bcl-2 family proteins, which are located in the outer membrane of the mitochondria, endoplasmic reticulum and nuclear envelope, are potent anti-apoptotic proteins (Ola et al.2011). Caspase-3, which is recognized as the main effector caspase, is involved in both intrinsic and extrinsic apoptosis pathways, causing the fragmentation of DNA which leads to apoptosis (Riedl and Shi 2004).
Development of neoantigens: from identification in cancer cells to application in cancer vaccines
Published in Expert Review of Vaccines, 2022
Nasim Ebrahimi, Maryam Akbari, Masoud Ghanaatian, Parichehr Roozbahani moghaddam, Samaneh Adelian, Marziyeh Borjian Boroujeni, Elnaz Yazdani, Amirhossein Ahmadi, Michael R. Hamblin
Necroptosis is an alternative mode of programmed cell death with features of both apoptosis and necrosis. In a similar manner to necrosis, it is considered to be pro-inflammatory, but is more effective in triggering the maturation of dendritic cells, cross-priming of cytotoxic T cells, and the secretion of IFN-gamma. This leads to better sensitization to tumor antigens contained within the necroptotic cancer cells [118]. Aaes et al. developed a method to produce necroptotic cells using direct dimerization of FADD combined with inducible expression of RIPK3 (receptor interacting protein kinase-3). These necroptotic cells enabled successful prophylactic vaccination of mice against CT26 colorectal tumors [118]. In another study by Turubanova et al. they used photodynamic therapy (PDT) mediated by two different photosensitizers, Photosens (PS) and Photodithazine (PD) against murine glioma GL261 and fibrosarcoma MCA205 cells. The type of cell death induced was analyzed by flow cytometry. The results indicated that PDT with PS or PD were novel ICD inducers, and could be used as a potential approach to prepare cancer vaccines [119].
The herbicide paraquat-induced molecular mechanisms in the development of acute lung injury and lung fibrosis
Published in Critical Reviews in Toxicology, 2021
Rajasekaran Subbiah, Rajnarayan R. Tiwari
A programmed cell death (apoptosis) is a tightly regulated and highly conserved cell death process during which a damaged or infected or potentially neoplastic cell undergoes self-destruction (Elmore 2007). So, tight regulation of apoptosis is critical for maintaining normal cellular homeostasis. However, deregulated apoptosis has been linked to several pathologies, including chronic inflammation and fibrosis (Favaloro et al. 2012). Many factors, including ROS, DNA damage, and receptor-mediated signals, are reported to activate apoptosis (Solano-Gálvez et al. 2018). Three main signaling pathways mediate programmed cell death. These include an extrinsic pathway involving the interaction of death ligands of the TNF family (TRAIL/Apo2L) with their appropriate cell surface death receptors (TRAIL-R1 (DR4), TRAIL-R2 (DR5), TRAIL-R3 (DcR1), and TRAIL-R4 (DcR1)) or intrinsic pathway involving mitochondria (through Bcl-2 family proteins) or endoplasmic reticulum (ER) stress pathway (Solano-Gálvez et al. 2018).