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Bacteria
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
In obligate aerobic organisms the TEA is oxygen and the process is called aerobic respiration. This type of metabolism, where oxygen is an obligatory nutrient, is found in all animals and in aerobic bacteria. In some obligate aerobes (e.g., hydrogen oxidizing bacteria), the organism must grow by aerobic respiration but the organism is sensitive to oxygen above about 0.2 atmospheres. These bacteria, known as microaerophilic, contain an essential enzyme that is inactivated by oxygen (e.g., hy-drogenase). A variation unique to the microbial world is that some bacteria have the capacity to substitute inorganic chemicals (i.e., carbonate, nitrate, nitrite, sulfate) in place of oxygen as their TEA and grow in the absence of oxygen. This process is called anaerobic respiration. An additional variation, known as fermentation, is found in other microbes that have the capacity to transfer electrons to partially reduced organic compounds in the absence of a complete electron transport system and derive energy from the process. For example, some fermenters are unable to synthesize cytochromes which are essential components of an electron transport system.
Inflammation and Infection
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Judith Hall, Christopher K. Harding
Pathophysiology:Endotoxins released by gram-negative bacteria.Inflammatory cells infiltration (neutrophils, macrophages, plasma cells).Cytokine release: TNFα, IL-2, IL-6, IL-8.Activation of kinin complement and the fibrinolytic system.Anaerobic respiration and lactic acid accumulation.Metabolic acidosis → vasoconstriction and cellular membrane dysfunctionMicrovascular injury and tissue ischaemia.Hypotension (shock) from cytokine-mediated vasodilatation.
Biochemical and Metabolic Limitations to Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Ultimately, oxygen bioavailability is crucial at a biochemical level, as oxygen is the final electron acceptor in the process of cellular respiration. This allows oxidative phosphorylation and generation of adenosine triphosphate (ATP) (biochemical energy), whereas a deficient matching of oxygen delivery to the working mitochondria results in reliance on anaerobic respiration. Both aerobic and anaerobic respiration result in the build-up of biochemical intermediates, which limit performance. The biochemical and metabolic limits of athletic endurance and performance can be essentially boiled down to three abilities:The ability to match oxygen requirement to mitochondrial respiration in a temporally and spatially specific mannerThe ability to prevent accumulation of by-products of anaerobic and aerobic respiration, which are detrimental to performanceThe ability to efficiently metabolize readily available fuel or metabolites
Targeted mitochondrial drugs for treatment of myocardial ischaemia-reperfusion injury
Published in Journal of Drug Targeting, 2022
Jin-Fu Peng, Oluwabukunmi Modupe Salami, Cai Lei, Dan Ni, Olive Habimana, Guang-Hui Yi
It is no exaggeration to use the love-hate triangle to describe the association between mitochondrial Ca2+, ATP, and reactive oxygen species (ROS) (Figure 1). Healthy mitochondria generate ATP molecules through an aerobic process known as oxidative phosphorylation (OXPHOS) [9,10], with ROS being an inevitable by-product of OXPHOS [11]. Besides, mitochondrial damage during myocardial ischaemia can damage OXPHOS and lead to excessive production of ROS and insufficient bioenergy [9,12]. Due to the decrease in ATP synthesis, anaerobic respiration produces more lactic acid, and the PH value of myocardial cells decreases. During the process of reperfusion to restore physiological PH, H+/Na+ exchange occurs, and the subsequent Na+/Ca2+ exchange in the mitochondria will cause calcium overload in the mitochondria [13,14]. The mitochondrial permeability transition pore (mPTP) is a non-selective and high-conductivity channel located in the inner mitochondrial membrane [15,16] (Figure 1). The mPTP keeps a closed conformation during ischaemia and an open conformation after myocardial reperfusion [17]. The abnormal opening of mPTP leads to the breakdown of mitochondrial membrane potential, some pro-apoptotic factors such as ROS and cytochrome c will be released into the cell, which will lead to cardiomyocyte apoptosis in the mitochondrial pathway, then, abnormal mitochondrial quality occurs.
Dimensions of inflammation in host defense and diseases
Published in International Reviews of Immunology, 2022
In mammals, lactate is a metabolic by-product of anaerobic respiration, a glycolytic pathway that ensures quick energy replenishment in the form of adenosine triphosphate (ATP) for the cells and prevention of muscle fatigue. Lactate acts as a circulating fuel in the blood that goes to the liver and is converted into pyruvate by the enzyme lactate dehydrogenase. Pyruvate is then converted into glucose via a metabolic pathway known as gluconeogenesis in the liver. Notably, lactate production increases when demand for ATP increases. In the past three decades, lactate has also been proved to be a very important signaling molecule that regulates various signaling pathways including inflammation-associated immune pathways. In this special issue, Zhou et al. [1] and Luo et al. [2] shed light on how endogenous lactate regulates inflammation in various immunological events, such as via macrophage polarization, T-cell immune dysfunction and its link with infectious and noninfectious diseases such as tumors. These two articles will be of interest to a broad readership in the field of immunology, as well as researchers investigating metaflammation and immunometabolic disorders and those in associated fields (Figure 1).
α-Hederin inhibits the growth of lung cancer A549 cells in vitro and in vivo by decreasing SIRT6 dependent glycolysis
Published in Pharmaceutical Biology, 2021
Cong Fang, Yahui Liu, Lanying Chen, Yingying Luo, Yaru Cui, Ni Zhang, Peng Liu, Mengjing Zhou, Yongyan Xie
Reprogramming energy metabolism is a hallmark of cancer. Energy metabolism is the process in which energy is generated from nutrients, released, stored, and consumed by organisms or living cells. Energy metabolism is divided into glucose metabolism, protein metabolism, and fat metabolism. Under normal conditions, cells generate energy primarily via aerobic respiration. When the oxygen content is insufficient, cells perform glycolysis to generate energy. This process is called anaerobic respiration. Unlike normal cells, tumour cells generate energy primarily via glycolysis, even under aerobic conditions, a phenomenon known as the Warburg effect. Glycolytic capacity is characterized by rapid productivity and low efficiency. The rapid proliferation of tumour cells requires rapid energy consumption. Meanwhile, the lactic acid generated by glycolysis creates an acidic environment for tumour cells, which is conducive to their growth and leads to their rapid proliferation (Zhao et al. 2014; Potter et al. 2016). Sirtuin 6 (SIRT6) protein is a chromatin binding factor that was initially described as an inhibitor of gene instability (Mostoslavsky et al. 2006). During energy metabolism, SIRT6 regulates the fat and glucose metabolism, which is a key regulator of energy stress and is closely related to the process of tumour growth (Sebastián and Mostoslavsky 2015). With the metabolic profile used for energy production is elucidated, regulating tumour metabolism is a new therapeutic strategy to inhibit tumour growth (Zhang and Yang 2013).