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Introduction to Oxidative (Eu)stress in Exercise Physiology
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Gareth W. Davison, James N. Cobley
Reactive nitrogen species (RNS) is a term used to explain the process of an unpaired electron residing on a nitrogen molecule (Halliwell and Gutteridge, 2015). Common RNS include nitrogen dioxide , nitrous acid (HNO2), dinitrogen trioxide (N2O3), nitroxyl anion (NO−), nitric oxide and peroxynitrous acid (ONOOH). Of these, perhaps the most widely known is .
Nitric Oxide as a Signaling Molecule in the Systemic Inflammatory Response to LPS
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
The cellular redox changes that accompany gram-negative sepsis are now recognized as important events that determine not only cell survival, but the nature of cellular responses to LPS challenge. Both reduction products of oxygen and NO-derived reactive nitrogen species are produced by LPS-activated cells and elicit similar adaptive responses. Nitric oxide has been shown to S-nitrosylate transcription factors in vitro, especially those of the NF-κB and Fos/Jun families, and alter gene expression. There is no reason to believe that other NO-sensitive signaling molecules within LPS pathways will not be described. However, we currently lack a detailed understanding of the significance of these findings. For example, studies that would causally link the (in)activation of NF-κB by NO with the impaired expression of specific genes are needed. What is the molecular basis for defining a redox-sensitive, LPS-activated response? What are the endogenous effects of NO production, and how do they relate to studies with NO donors, which are less than perfect models of NO production and reactivity in vivo (60)? What are the roles of cellular antioxidant systems in regulating responses to LPS, and which are important in preventing or correcting NO-induced redox stress? Does glu tathione also serve as a signaling sensor that transmits an oxidative signal in the NO cascade?
Basic Facts about Oxidative Stress, Inflammation, and the Immune System
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Reactive nitrogen species (RNS) are represented by nitric oxide (NO•). NO is synthesized by the enzyme nitric oxide synthase from L-arginine. NO• can combine with superoxide anion to form peroxynitrite, a powerful oxidant.
How changing environments alter the microbial composition and ecological response in marine biofilms: a mini review
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Marine nitrogen deposition involves the atmospheric input of reactive nitrogen into the marine environment. The process by which reactive nitrogen is transferred from the atmosphere to the ocean affects the pH, nutrient status and biofilm formation of the marine environment. Nitrogen is the most important element that tends to alter primary productivity of marine environment due to its crucial role in marine biogeochemistry and its interrelation with other biogeochemical cycles such as carbon cycle. In marine environment, nitrogen ranges in form from NH4 and NO3 which are in reduce form and fully oxidized form, respectively. This is the reason why nitrogen could act as both electron donor and acceptor in marine environment. The alteration of marine environment caused by GHGE tends to have negative effect on marine biota. It is thereby important to study the role of marine biofilm in marine nitrogen deposition. The marine nitrogen deposition process involves different microbial transformations, and enzymes are found in the organism forming marine biofilm. These processes of transformation of nitrogen compounds in the marine environment tend to have important effects on the stability of nitrogen in marine environment. The present study reports processes involved in marine nitrogen deposition and the role of marine biofilm in the process of nitrogen transformation and deposition. The present study is based on marine-fixed nitrogen, marine-retained nitrogen and marine loss nitrogen.
International expert group collaboration for developing an adverse outcome pathway for radiation induced leukemia
Published in International Journal of Radiation Biology, 2022
Dmitry Klokov, Kimberly Applegate, Christophe Badie, Dag Anders Brede, Fieke Dekkers, Melis Karabulutoglu, Yevgeniya Le, Eric Andreas Rutten, Katalin Lumniczky, Maria Gomolka
The molecular initiating event (MIE) for IR as a stressor is ‘Deposition of energy’ (Alloni et al. 2014). A single photon or a particle of ionizing radiation may cause multiple ionization events within a cell and interact with both water and biomolecules. Energy depositing onto water causes production of reactive oxygen species that by chemical reaction leads to formation of reactive nitrogen species. Therefore, the KE1 was called ‘Production of RONS, Increase’ (RONS stands for Reactive Oxygen and Nitrogen Species). These radicals contribute to two important branches leading to the development of AML (Figure 1). The first branch starts with the second key event (KE2), ‘DNA Damage, Increase’ and includes DNA damage produced by both RONS (KE1) and energy deposition (MIE) (Goodhead 1994; Lomax et al. 2013). Depending on the extent and complexity of the damage, cells activate a number of defence mechanisms such as DNA Damage Response (DDR). However, DNA damage repair can be error prone, so that inadequate DNA repair (KE3) leads to accumulation of mutations. Such mutations or chromosomal aberrations can affect or inactivate critical genes (KE4) (Genovese et al. 2014; Jaiswal et al. 2014) within hematopoietic stem cells (HSCs). Increased proliferation (KE5) of the affected HSC further leads to the formation of preleukemic myoblast cells that are capable of clonal expansion (KE5) (Verbiest et al. 2018).
Molecular and cellular pathways in colorectal cancer: apoptosis, autophagy and inflammation as key players
Published in Scandinavian Journal of Gastroenterology, 2022
Lei Yu, Miao-Miao Zhang, Ji-Guang Hou
Inflammation plays a prime contributory role, having a significant influence in the generation of CRC, as supported by the increased prevalence of CRC in patients suffering from ulcerative colitis and Crohn's disease, marked by chronic inflammation [52]. Thus, Non-steroidal anti-inflammatory drugs (NSAIDs) have been reported as playing a preventive therapeutic role in CRC. Chronic inflammation, could lead to CAC and CRC, involving the generation of pro-inflammatory cytokines, mutations in the APC, p53, K-ras tumor suppressor genes, together with dysregulated apoptotic machinery, enhanced premalignant proliferation and often genomic instability [53,54]. This could trigger tumorigenesis and colon carcinogenesis. Although inflammation may not initiate sporadic colorectal carcinogenesis, chronic inflammation may undergo induction following tumor formation, where the surrounding tumor inflammatory microenvironment triggered mutations and epigenetic alterations. This may have resulted in oxidative stress, reactive nitrogen species generation and DNA damage.