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Exercise Redox Signalling
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Ruy A. Louzada, Jessica Bouviere, Rodrigo S. Fortunato, Denise P. Carvalho
Finally, the importance of modulating the redox environment status was recently confirmed by the discovery of an endogenous factor capable of promoting “reductive stress” that counteract the physiological ROS bursts induced by exercise (Takamura, 2020). Elegantly, Musi et al. demonstrated that selenoprotein P (SEPP1) enables communication between the liver and muscle to upregulate GPX1, which maintains a reduced intracellular environment that is related to a lack of ROS-induced AMPK/PGC-1α activation following physical exercise. As a result, the beneficial effects of exercise are hampered in some obese patients with high circulating levels of SEPP1 (Misu et al., 2017).
Hypoxia, Free Radicals, and Reperfusion Injury Following Cold Storage and Reperfusion of Livers for Transplantation
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Ronald G. Thurman, Wenshi Gao, Henry D. Connor, Sigrid Bachmann, Robert T. Currin, Ronald P. Mason, John J. Lemasters
During ischemia and hypoxia, reduced electron carriers accumulate in the respiratory chain of mitochondria. These carriers are usually oxidized in the aerobic state; however, in the reduced or partially reduced state (e.g., ubisemiquinone), they can form superoxide by reacting directly with molecular oxygen86,100 (Figure 2). Cytochrome bc1 (Complex III) and probably NADH-ubiquinone oxidoreductase (Complex I) are major sources of oxygen radicals in ATP-depleted hepatocytes.95 Therefore, reductive stress due to anoxia predisposes hepatocytes to oxygen radical formation upon reoxygenation.25,95,101 Relative but not absolute oxygen deprivation in cells and tissues is caused by respiratory failure, hypotension, and regional hypoperfusion. In these states, individual cells may be completely anoxic, mildly hypoxic, or even normoxic. Oxygen radical formation during incomplete or intermittent oxygen depletion may contribute to lethal cell damage to a greater extent than during absolute ischemia followed by reperfusion.
Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Both OS and reductive stress trigger oxidative shielding. Functional and metabolic defects occur in the cell before the increase in ROS and oxidative changes. According to Naviaux, ROS are the response to the triggering of the disease, not the cause.214 Environmental factors are the triggering agents of disease coupled with the hereditary defects. The environmental triggers have been shown throughout the body, the most common being natural gas, pesticides, mycotoxins, and car exhaust. These all need to be shielded.
Oxidative versus reductive stress: a delicate balance for sperm integrity
Published in Systems Biology in Reproductive Medicine, 2023
Niloofar Sadeghi, Guylain Boissonneault, Marziyeh Tavalaee, Mohammad Hossein Nasr-Esfahani
Cellular redox is defined as a balance between pro‐oxidants and antioxidants. As previously reported in the literature, cellular pro-oxidants comprise ROS, generated in the form of superoxide anion (O2•‐), hydrogen peroxide (H2O2) from the electron transport chain (ETC), or mitochondrial enzymes such as NADPH-dependent oxidase 4 (NOX4) and α-ketoglutarate dehydrogenase (α-KGDH) (Figure 1) (Handy and Loscalzo 2012; Xiao and Loscalzo 2020). That is why cells contain a broad range of antioxidants, including enzymatic antioxidants (superoxide dismutases (SOD1‐3), catalase, glutathione peroxidases (GPx1‐8), thioredoxins (Trx1‐2), and peroxiredoxins (Prx1‐6) and non-enzymatic antioxidants (GSH, α‐tocopherol, Folic acid, Bilirubin, uric acid, Carotenoids, ascorbate, etc.) to neutralize cellular oxidants (O'Flaherty 2014; Cheng and Ko 2019; Xiao and Loscalzo 2020; Rashki Ghaleno et al. 2021). However, cellular functions such as cell signaling, proliferation, and differentiation require a steady‐state level of cellular pro-oxidant under physiological conditions. Hence, any impairment in pro‐oxidants and antioxidants status leads to either oxidative or reductive stress known as redox stress (Pérez-Torres et al. 2017).
Systematic review of antioxidant types and doses in male infertility: Benefits on semen parameters, advanced sperm function, assisted reproduction and live-birth rate
Published in Arab Journal of Urology, 2018
Antioxidants are biological or chemical compounds that scavenge free radicals, neutralise their effect and halt the chain reaction leading to OS in body tissues. To overcome OS in infertile patients, antioxidants have been a common prescription for men seeking fertility supported by their relatively inexpensive and easily accessible nature. However, several studies have shown conflicting results for the effect of the antioxidant therapy on male fertility. Whilst a number of studies conveyed a favourable effect on basic semen parameters, advanced sperm function tests, and pregnancy rates; others failed to confirm such an effect or even reported a negative influence on male fertility. This may be attributed to the extensive heterogeneity that characterises the studies conducted on this particular topic. Furthermore, the ideal balance of the redox system necessary for optimal sperm function is not known and overconsumption of antioxidants may result in reductive stress that could cause detrimental effects on human health and well-being. Impairment of mitochondrial activity [43], reduction in blood–brain barrier permeability [44], and attenuation of endothelial cell proliferation [45] are consequences that have been reported to occur secondary to reductive stress.
The potential association between metabolic syndrome and risk of post-surgical adhesion
Published in Archives of Physiology and Biochemistry, 2023
Gordon A Ferns, Milad Shahini Shams Abadi, Mohammad-Hassan Arjmand
In addition to alterations in coagulation and activation of platelets, MetS can contribute to inflammation and oxidative stress. Several studies have shown associations between the various aspect of MetS and inflammation, as shown by its relationship with inflammatory markers such as C reaction protein (CRP), TNF-α, fibrinogen, and IL6 (Hotamisligil et al. 1995, Pannacciulli et al. 2001, Ford 2003). The high visceral fat in MetS leads to the increased release of inflammatory cytokines into circulation that stimulate the production of CRP, in this way various investigations demonstrated that obesity is related to chronic inflammation (Yudkin et al. 1999). Adipokines secreted from adipose tissues up-regulate molecular mechanisms that promote the expression of resistin (an inflammatory adipokine), TNF-α, IL6, and CRP. Recent studies have shown that that resident macrophages in adipose tissue are a source of inflammatory factors of visceral fat tissues (Xu et al. 2003). Also, it’s suggested that adipokines from visceral fat are responsible for insulin resistance (Pittas et al. 2004). Individuals with high visceral fat are more exposed to insulin resistance and at a greater risk of type 2 diabetes mellitus. Increased levels of adipokines have been implicated as a possible link between insulin resistance and inflammation (Juhan-Vague et al. 1991). deregulated lipid and carbohydrate mechanism in MetS increase production of superoxide O2– through increase electron carrier of the mitochondria electron transport chain (Rudich et al. 2007). Metabolic effects associated with MetS increase the production of reactive oxygen species (ROS) such as superoxide generation through over-produce of NADH molecule by different pathways like the glycolytic and Polyol pathway (Liu et al. 2002, Chung et al. 2003). An excessive amount of NADH causes reductive stress leads to oxidative stress. NADH making ROS by transport electron in complex 1 of the electron transport chain in mitochondria. Additionally, hyperglycaemia in MetS leads to over-production of Advanced Glycation End Products (AGEs) that stimulates NOX activation for ROS formation and oxidative stress (Guimarães et al. 2010). NAD (P) H oxidase (NOX enzyme) is one of the main sources in the cellular generation of ROS in almost all types of cells special phagocytic cells, to kill microorganisms. Oxidative stress is a result of ROS formation in MetS induces inflammation and production of inflammatory cytokines by immune cells, which are associated with post-surgical adhesion pathogenesis (Fortin et al. 2015). Moreover, insulin resistance and diabetes lead to fibroblasts dysfunction that has a key role in a normal wound healing process. in vitro study showed elevated glucose levels promote adhesion fibroblasts in compare with normal fibroblast lead to abnormal healing process and increase the risk of post-surgical adhesion (Rizk et al. 2006). Difference in expression and differential response of adhesive fibroblasts to hyperglycaemia suggest that insulin resistance and MetS can able to develop post-surgical adhesion.