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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.
Radiobiology of Tumours
Published in W. P. M. Mayles, A. E. Nahum, J.-C. Rosenwald, Handbook of Radiotherapy Physics, 2021
Gordon Steel, Catharine West, Alan Nahum
When cells are fatally damaged by radiation, they do not die immediately; after a dose-dependent delay in progression through the cell cycle, they usually proceed to mitosis. Damaged cells often fail to complete mitosis, or they may go through one or more further cell cycles before getting stuck at a subsequent cell division (see Figure 6.1). However, lymphocytes as well as some other cell types die before reaching mitosis. This is called intermitotic cell death. It is closely related to what is called programmed cell death or apoptosis (‘self-killing') (Haimovitz-Friedman et al. 1996). Radiation-induced autophagy (‘self-eating') can also contribute to cell killing. In autophagy, cells recycle proteins to help them survive under conditions of stress and as a protective mechanism following damage caused by agents such as radiation. Autophagy tends to block the induction of apoptosis, and apoptotic pathways can inhibit autophagy. However, proteins released during the process of autophagy can induce apoptosis or necrosis, and when autophagy degrades the cytoplasm excessively, it leads to an autophagic cell death. Cross-talk between autophagy and apoptosis pathways impacts on the clearance of dying cells and the immune recognition of dead cell antigens (Mariño et al. 2014). The implication of this is that the type of cell death that an individual tumour undergoes might impact on the ability of a host immune response to eradicate the last remaining clonogenic cells (see Section 6.4.2) – thus, tumour response to radiation is not always solely about clonogenic cell survival.
Recent Progress in Cancer Thermal Therapy Using Gold Nanoparticles *
Published in Valerio Voliani, Nanomaterials and Neoplasms, 2021
Nardine S. Abadeer, Catherine J. Murphy
Traditional cancer hyperthermia results in thermal damage and temperatures in the surrounding extracellular matrix ranging from 41°C to 48°C. Cancer cell death from traditional hyperthermia can result from damage to the cell membrane, denaturation of intracellular proteins, damage/impairment of RNA/DNA synthesis, changes in gene expression, and induction of cell death via apoptosis [94]. Heating may also increase susceptibility or sensitize cancer cells to other cancer treatments, including radiation and chemotherapy [95]. The effects of photothermal heating on cancer cells can be similar to traditional hyperthermia. However, as demonstrated by the ongoing debate in the literature between death by apoptosis or necrosis, one singular mechanism may not be sufficient to describe the effects of photothermal therapy with gold nanoparticles [96]. Apoptosis, also called programmed cell death, is characterized by membrane blebbing, nuclear fragmentation, and apoptotic body formation. The apoptotic bodies are eventually recognized by the immune system and are removed by phagocytes. Necrosis, originally thought to be a more passive form of cell death, results from toxicity or damage and is characterized by membrane collapse and cell swelling, resulting in rupture and release of the cellular contents [97]. The following reports in this section on observed mechanisms of cell death after photothermal therapy are summarized in Table 3.3.
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).
Effects of Monobenzyl ether of hydroquinone on 3T3 mouse fibroblast viability and ultrastructure
Published in Ultrastructural Pathology, 2021
Aslı Erdoğan, Hasan Serdar Mutlu, Sibel Doğan, Tuğba Kotil
There are three main types of cell death: apoptosis, necrosis and autophagy.20 Of these, apoptosis is referred to as programmed cell death and occurs in a way that causes minimal damage to surrounding tissues. Morphological markers of apoptosis are cell membrane blebbing, fragmentation in the nucleus, chromatin condensation, formation of apoptotic bodies, and reduction in cell size.21,22 Necrosis, however, is cell death that occurs as a result of unexpected damage such as hypoxia and inflammation and is characterized by swelling of organelles, disruption of the integrity of the cell membrane, and release of cell contents, leading to inflammation.23 In autophagic cell death, double-membrane autophagosome (autophagic vacuole) structures containing damaged organelles and other cytoplasmic components are observed. Autophagosomes then fuse with the lysosome and are used in the production of new cell structures or organelles by the destruction of the macromolecules they contain, or they can be processed as an energy source.24,25 In this context, although autophagy functions as a mechanism that can ensure the survival of the cell by degradation of the cellular components, it is also a process that can lead to cell death.26,27 Although the main mechanisms of the three basic cell death types are different from each other, signaling pathways are interrelated and these pathways can be activated simultaneously.21,28 In addition, apart from the three main mechanisms of cell death, many different new mechanisms have been described in recent years.29,30
Assesment of hematotoxic, oxidative and genotoxic damage potentials of fipronil in rainbow trout Oncorhynchus mykiss, Walbaum
Published in Toxicology Mechanisms and Methods, 2021
Arzu Uçar, Veysel Parlak, Aslı Çilingir Yeltekin, Fatma Betül Özgeriş, Özge Çağlar, Hasan Türkez, Gonca Alak, Muhammed Atamanalp
The results showed that 8-OHdG content in the blood tissue of FP treated fish was increased due to dose increase. It is clear that this increase is a response to oxidative damage. Apoptosis is a regular and programmed cell death that occurs in physiological or pathological processes. The mechanism of apoptosis is highly complex and is activated by two major pathways, "extrinsic" and "intrinsic". Both pathways of apoptosis work with caspase (cysteinyl aspartate specific protease) activation. After receiving intrinsic or extrinsic signals, the cells follow the course of caspases mediated pathways. The mitochondria contain cytochrome-c under normal conditions to form ATP. Released cytochrome-c in mitochondrial stress conditions plays an important role in caspase-3 activation in apoptotic cell death (Elmore 2007; Bildik and Bayar 2018). As a final step, caspase-3 activation triggers the activation of cell content proteolysis and DNA fragmentation (Wolf et al. 1999). Therefore, caspase-3 is considered a universal indicator of an apoptotic cell (Ostapchenko et al. 2019). In this study, although Caspase-3 activity increased in blood tissue due to high dose, this change was not statistically significant. The high level of oxidative stress caused by ROS formation stimulates various cell signaling pathways, often associated with apoptosis. Induction of apoptosis by environmental toxicants is associated with a change in the antioxidant defense system leading to oxidative stress in the redox balance. It can be said that this change causes oxidative stress, DNA damage, and apoptosis in fish.