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Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Apoptosis, also known as Programmed Cell Death, is induced in cells in response to physiological or pathological changes in order to eliminate aged cells, or those with extensive genetic mutations that might pose a risk of transforming into cancer cells if not eradicated. There are two predominant apoptotic pathways, the first being the intrinsic/mitochondrial pathway which is regulated by the Bcl protein family. This initially results in various stimuli which trigger increased mitochondrial membrane permeability to release apoptogenic factors, leading to membrane disruption and mitochondrial dysfunction. This results in activation of apoptogenic proteases including caspase-3 and -9, and also the expression of Death Receptors (i.e., DR4 and DR5) on the cell surface. Caspase enzymes also play vital regulatory roles in cell protein turnover via several activating and deactivating mechanisms, with nine different caspases involved in apoptotic pathways. The extrinsic apoptotic pathway is stimulated via binding of a ligand from the TNF superfamily to a Death Receptor on the cell surface. Once bound, the ligand undergoes trimerization which stimulates recruitment of adaptor proteins to their cytosolic Death Domains, such as FasL/FasR, TNFα/TNFR1, and TRAIL/TRAILR1 or TRAILR2.
Structure, Function and Evolutionary Aspects of Mitochondria
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Puja Agarwal, Mehali Mitra, Sujit Roy
Mitochondria contain two membranes – one inner and the other mitochondrial membranes. The outer mitochondrial membrane acts as an outer boundary of the mitochondria whereas the inner mitochondrial membrane has some inward projections (Fig. 1) which are known as Cristae (Hoppins et al., 2011). The outer part of inner mitochondrial membrane is known as inner boundary membrane. This inner boundary membrane and cristae are joined together by narrow and tubular connections which are known as cristae junctions (Douce and Neuberger, 1989).
Liver, GI and Metabolism
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
Final metabolic pathway of cellular respiration that occurs on inner mitochondrial membraneTendency for electrons to be transferred from activated carriers (e.g. NADH – ‘loaded’ during CAC) to cascade of lower potential carriers (electron transfer chain)Process involves many enzymes, including those of cytochrome oxidase systemProton pumps in inner mitochondrial membrane are activated by flow of electrons through them pumping H+ ions out and creating gradient that generates ATP (via ATP synthase) by driving H+ ions back across inner membraneRequires oxygen and results in liberation of 30 ATP molecules per molecule of glucose
Antioxidant activity of calcitriol reduces direct methamphetamine-induced mitochondrial dysfunction in isolated rat heart mitochondria
Published in Toxin Reviews, 2022
Ahmad Salimi, Morteza Minouei, Mohsen Niknejad, Elham Mojarad Aylar
Mitochondrial membrane potential is a main indicator of mitochondrial function and viability. Mitochondrial membrane potential in the isolated cardiac mitochondria was measured by flow cytometry with the fluorescent probe rhodamine 123. Compared to the control group, the ratio of fluorescence intensity of rhodamine 123 was markedly increased (p < 0.001 and F = 18) in the isolated cardiac mitochondria treated with 250 µM methamphetamine for 1 h, indicating mitochondrial damage and a drop in ΔΨm. Calcitriol cotreatment (2.5 and 5 µM) significantly inhibited the methamphetamine-induced loss of ΔΨm in the isolated cardiac mitochondria (p < 0.001). Cyclosporine A, as a blocker of the MPT pore opening, was used for confirmation of the inhibitory effect of calcitriol on the MPT pore opening (data not shown) (Figure 3).
Targeting mitochondria in dermatological therapy: beyond oxidative damage and skin aging
Published in Expert Opinion on Therapeutic Targets, 2022
Tongyu C Wikramanayake, Jérémy Chéret, Alec Sevilla, Mark Birch-Machin, Ralf Paus
Before going into details, it may be useful to recapitulate some essentials of mitochondrial biology. Reminiscent of their endosymbiont past, mitochondria are surrounded by two phospholipidic membranes, the outer mitochondrial membrane (OMM) and the inner mitochondrial membrane (IMM), which divide the organelle into two compartments, the matrix and the intermembrane space (IMS) [212] (see Figure 2 for details). Mitochondria contain their own DNA (mtDNA) and translation system. The location of mtDNA in the matrix, in close proximity to the ETC, a major source of reactive oxygen species (ROS), makes it particularly vulnerable to oxidation, resulting in mtDNA mutations that could contribute to the pathogenesis of cancer, diabetes and aging [213]. Mutations in mtDNA are functionally recessive – a biochemical phenotype is only observed when the levels of mutated mtDNA reach a critical threshold, and the proportion of mutated versus wild-type mtDNA has a strong impact on the severity of the pathological phenotypes. Coenzyme Q (CoQ10), a ROS scavenger, and mitochondrial sirtuins (SIRT3 and SIRT4) have been implicated in maintaining mitochondrial health [109,214].
Preadministration of high-dose alpha-tocopherol improved memory impairment and mitochondrial dysfunction induced by proteasome inhibition in rat hippocampus
Published in Nutritional Neuroscience, 2021
Ali Nesari, Mohammad Taghi Mansouri, Mohammad Javad Khodayar, Mohsen Rezaei
The present study demonstrated that inhibition of the proteasome induces oxidative stress, evidenced by an increase in ROS and MDA levels. Dysfunction and damage of the mitochondrial membrane were also present. Excess ROS contributed to the pathogenesis of various diseases that damage all cellular components, including DNA, proteins and lipids and affects enzyme functions, membrane structures and gene expression [5,77]. Lipid peroxidation (LPO) is a consequence of free radical-mediated damage to membranes and generates a number of secondary products that increase neurotoxicity. Numerous studies have demonstrated increasing LPO in the brain of patients with Alzheimer’s disease [78]. MDA is mutagenic, carcinogenic and one of the reactive products resulted from the oxidative stress that serves as a major determinant of LPO [79–81].