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Biological Correlates of Microwave
Published in Jitendra Behari, Radio Frequency and Microwave Effects on Biological Tissues, 2019
ROS are produced intracellularly through multiple mechanisms and depending on the cell and tissue types, the major sources being the regular producers of ROS: NADPH oxidase (NOX) complexes in cell membranes. One of these, i.e., mitochondria converts energy for the cell into a usable form, adenosine triphosphate (ATP). The process by which ATP is produced, called oxidative phosphorylation involves the transport of protons (hydrogen ions) across the inner mitochondrial membrane by means of the electron transport chain (Hall et al. 1996). If too much damage is done to mitochondria, a cell undergoes apoptosis (programmed cell death). The cellular stress response is a specific response of individual cells, and stress proteins are the chemical agents that also serve as markers of the magnitude of the external agent.
Mammalian Cell Physiology
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
The generation of ATP in animal cells is accomplished through the mitochondrial ETC located in the inner mitochondrial membrane. It consists of a multienzyme complex which accepts reducing equivalents from NADH and FADH2 and transfers them through several oxidation-reduction reactions to molecular oxygen, with the subsequent formation of water and ATP (179). The transfer of reducing equivalents occurs down an electrochemical potential gradient which liberates energy through exergonic redox reactions. This liberated energy is used for the synthesis of ATP (179). Steady-state systems which balance the production and utilization of energy in the form of ATP exist in all living organisms. A precise dynamic balance is maintained between reactions that produce ATP within cells and those that use it. As a result, the concentration of ATP within cells should remain constant under nonlimiting conditions. The rate of ATP synthesis in man can vary from 0.4 g ATP/min/kg body weight at rest to 9.0 g ATP/min/kg body weight during strenuous exercise (179). This wide variation in rate of synthesis illustrates the capacity of cells in vivo to adjust to substantial utilization of ATP for work.
Mechanisms of Nanotoxicity to Cells, Animals, and Humans
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Belinda Wong Shu Ee, Puja Khanna, Ng Cheng Teng, Baeg Gyeong Hun
As the energy house of the cell, mitochondria supply most of the energy required in the form of ATP during cellular respiration. Mitochondria are the site of basal ROS generation in which electrons escape from ETC and react with oxygen molecules to form free radicals. Nanoparticle exposure can cause mitochondrial dysfunction, which leads to decreased ATP production but increased ROS generation, culminating in oxidative stress (Valko et al. 2007). For instance, AgNPs reduced the ATP content in IMR-90 and U251 cells due to damaged mitochondria (AshaRani et al. 2009). Mitochondrial depolarization is one of the mechanisms by which nanoparticles induce mitochondrial dysfunction. Mitochondrial membrane potential is generated in the inner mitochondrial membrane when protons are pumped into the intermembrane space. These protons will later flow back into the mitochondria via ATP synthase to generate ATP. Hence, maintaining mitochondrial membrane potential is essential for consistent energy production (Chen 1988). Decreased mitochondrial membrane potential is an indicator for its depolarization and mitochondria malfunction. TiO2 NP exposure in primary rat cortical astrocytes reduced the mitochondrial membrane potential along with oxidative stress build-up in cells (Wilson et al. 2015). Similarly, iron oxide nanoparticles depolarized mitochondria membranes in a dose-dependent manner in A549 cells (Khan et al. 2012). These observations suggest that nanoparticles damage mitochondria. Decreased ATP contents and mitochondrial membrane depolarization are the signs of damaged mitochondria and can lead to oxidative stress. Following these events, the damaged mitochondria can be removed via mitophagy. Alternatively, affected cells can activate mitochondrial-mediated apoptosis.
Diazinon impairs bioenergetics and induces membrane permeability transition on mitochondria isolated from rat liver
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Camila Araújo Miranda, Anilda Rufino de Jesus Santos Guimarães, Paulo Francisco Veiga Bizerra, Fábio Erminio Mingatto
Mitochondria are responsible for synthesis of almost all of the ATP that is required for maintaining cellular structure and function. The proton motive force, whose major impetus is the membrane potential (ΔΨ), which is generated by electron transport along the respiratory chain in the inner mitochondrial membrane, drives ATP synthesis via oxidative phosphorylation (Mitchell 1961). Experimental evidence indicates that mitochondria represent a critical and preferred target for the action of drugs and toxins (Meyer et al. 2013). The toxic effects on mitochondria might occur through direct and indirect actions, leading to mitochondrial dysfunction including (1) changes in electron transport and oxidative phosphorylation, (2) increase in inner membrane permeability, (3) deregulation of calcium homeostasis, and (4) shifts in the redox state, as well as a series of other events that deplete ATP (Bizerra et al. 2018; Castanha-Zanoli et al. 2012; Dykens et al. 2008; Li et al. 2012; Nadanaciva et al. 2007; Oliveira et al. 2020).
Imidacloprid affects rat liver mitochondrial bioenergetics by inhibiting FoF1-ATP synthase activity
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Paulo F. V. Bizerra, Anilda R. J. S. Guimarães, Marcos A. Maioli, Fábio E. Mingatto
The effects of IMD on the bioenergetics of mitochondria isolated from rat liver were determined to assess the potential involvement of mitochondria in hepatic injury induced by this insecticide. Mitochondria are responsible for most of the energy generated and used by cells through oxidative phosphorylation (Nicholls and Ferguson 2013). The energy released by oxidation of substrates in the respiratory chain is utilized to transport protons across the inner membrane, supporting the proton motive force that drives ATP synthesis by FoF1-ATP synthase or complex V, which consists of two functional proteins: F1, situated in the mitochondrial matrix, and Fo, located in the inner mitochondrial membrane. Several investigators reported that various compounds are capable of producing alterations in oxidative phosphorylation (Bridges et al. 2014; Maioli et al. 2012; Wallace and Starkov 2000). Among these are inhibitors that interfere with ATP synthesis often operating in respiratory chain complexes or in FoF1-ATP synthase (Nicholls and Ferguson 2013; Zheng and Ramirez 2000).