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Synthetic Biology and Artificial Intelligence
Published in Lavanya Sharma, Mukesh Carpenter, Computer Vision and Internet of Things, 2022
According to Ron Weiss, a much more efficient technique for building relatively large DNA complexes without error is the so-called viral replacement technique [124]. This approach significantly expands the possibilities of building such complexes, which, according to Gibson, can be used to obtain vaccines using synthetic biology (SB). For example, it is known that the flu virus easily mutates, which is why we need a new vaccine every other year. With this method, it is possible to monitor mutations and synthesize a new virus very quickly to make a new effective vaccine against the flu virus. The experiments began with the mitochondrial genome because errors in its sequences lead to many diseases for which there is currently no real treatment. However, although we have already managed to create a synthetic mitochondrial genome, unfortunately, it is still not clear whether it is functional. However, it is obvious that it can correct disorders in cells with mitochondrial defects, which opens the way for designing treatments for various diseases [123–126].
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.
Putting a Cell Together
Published in Thomas M. Nordlund, Peter M. Hoffmann, Quantitative Understanding of Biosystems, 2019
Thomas M. Nordlund, Peter M. Hoffmann
The mitochondrion is a membrane-enclosed organelle found in most eukaryotic cells. The primary role of the mitochondrion is production of ATP, as reflected by the large number of proteins in the inner membrane for this task. ATP regeneration from ADP is done by oxidizing glucose, pyruvate, and NADH produced in the cytosol. Mitochondria generate most of the cell’s ATP, used as an almost universal source of molecular chemical energy in living systems. Production of ATP is remarkably large scale. In humans, the ATP turned over (generated, used, and regenerated) each day is the equivalent to the weight of the entire body!11 This turnover is so startling that the authors of that article close with the statement:Thus, although a camel cannot pass through the eye of a needle, it is extraordinary to imagine that every day its body weight’s equivalent in metabolites tunnel backward and forward through an integral membrane aperture ≈6 orders of magnitude smaller in diameter.
Genetic ethics and mtDNA replacement techniques
Published in The New Bioethics, 2021
Although genetic diseases associated with mutations in nuclear DNA have seen advancements in technologies to reduce inheritance, mtDNA replacement techniques have received slightly more resistance in the United States. The mitochondria are found within the cytoplasm and contain a subset of DNA (known as mtDNA) which spans about 16,500 building blocks accounting for about 0.1% of DNA (Genetics Home Reference 2017). Moreover, because mtDNA is responsible for energy conversion and present in virtually every cell in the human body, mutations in the sequence can cause a wide range of symptoms and diseases. Before discussing bioethical challenges related to mtDNA donation, an understanding of what types of diseases are associated with mutations and what mitochondrial donation entails is necessary.
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).
Scientific and Ethical Issues in Mitochondrial Donation
Published in The New Bioethics, 2018
Lyndsey Craven, Julie Murphy, Doug M. Turnbull, Robert W. Taylor, Grainne S. Gorman, Robert McFarland
Mitochondrial disease is a term that encompasses a diverse group of genetic disorders characterised by mitochondrial dysfunction. These disorders show vast clinical heterogeneity, with patients presenting at any age and with a wide range of clinical features often affecting multiple organ systems (Gorman et al.2016). The symptoms are usually progressive and can be associated with severe morbidity and early mortality. Inherited mitochondrial disease is genetically heterogeneous and can be caused by a number of different genetic mutations found in either the nuclear DNA, which is inherited from both parents, or the mitochondrial DNA (mtDNA), which is inherited from the mother only. This has made the clinical diagnosis of mitochondrial disease challenging. Recent advances in next-generation sequencing technology have significantly improved the diagnostic rate for both patients and their families (Craven et al.2017a) but unfortunately, progress in this area has not been matched with the development of effective treatments. There is currently no cure for mitochondrial disease and clinical management is focussed on symptom alleviation. This highlights the importance of obtaining a genetic diagnosis as it opens up the possibility of genetic counselling to understand the risks of transmitting mitochondrial disease and allows reproductive options to be considered that will reduce this risk.