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Exercise, Metabolism and Oxidative Stress in the Epigenetic Landscape
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Gareth W. Davison, Colum P. Walsh
In mammalian cell types, the production of ROS is regulated by enzymatic and non-enzymatic antioxidants. ROS, particularly H2O2, are important signalling molecules acting to induce transcription factor activation (e.g. Nrf2) and subsequent gene expression of a host of intracellular antioxidant enzymes (Figure 17.3). Gene expression of antioxidant enzymes can also be directly modulated by DNA methylation and post-translational histone modifications. For instance, the epigenetic regulation (methylation and histone changes) of superoxide dismutase 2 (SOD2) can affect promoter and enhancer sites, alongside other upstream regulatory elements (Cyr et al., 2013). Although the inter-relationship between exercise and epigenetic regulation of antioxidant enzymes is still in its infancy (Dimauro et al., 2020), Nguyen et al. (2019) found that glutathione peroxidase 1 (Gpx1) was hypomethylated following 3 months of exercise. This alteration was observed in the second exon of the Gpx1 gene and occurred alongside an increase in mRNA expression. In a more recent study, Sailani et al. (2019) demonstrated that protein levels of key antioxidant enzymes catalase (CAT) and superoxide dismutase 2 (SOD2) were enhanced with exercise, corresponding to a hypomethylation of SOD2 and CAT promoters (20% and 18%).
The Emerging Role of Exosome Nanoparticles in Regenerative Medicine
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Zahra Sadat Hashemi, Mahlegha Ghavami, Saeed Khalili, Seyed Morteza Naghib
Drug and toxicants injury is a significant cause of liver diseases (Fisher et al. 2015). Oxidative stress-related molecules are associated with liver damage and may arise after CCl4, H2O2, and acetaminophen treatment (de la Rosa et al. 2006). Yan and co-workers have demonstrated the necessity of glutathione peroxidase1 (GPX1) from the hUCMSC for the restoration of hepatic oxidant injury. The antioxidant and anti-apoptotic effects of administered exosomes saved mice from hepatic injury caused by carbon tetrachloride (CCl4). The underlying mechanism could be attributed to the detoxifying effect of hUCMSC-exosome-derived glutathione peroxidase1 (GPX1) CCl4, H2O2, and finally prohibited oxidative stress and apoptosis (Yan et al. 2017).
Antioxidants Neutralize Free Radicals
Published in Robert Fried, Lynn Nezin, Evidence-Based Proactive Nutrition to Slow Cellular Aging, 2017
SOD expression was elevated in the kidneys of females compared with males. GPx1 and glutathione reductase levels were also increased in older females compared with males. These findings indicate that a reduction in oxidative damage protection may be responsible for accelerated telomere shortening over time. This resulted in increased cellular senescence (aging), loss of renal function, and death in male rats (Tarry-Adkins et al. 2006).
Facing Back Pain with Wine and Physical Activity
Published in Journal of Investigative Surgery, 2022
Silvia Ravalli, Giuseppe Musumeci
A recent review published in the Journal of Investigative Surgery, discusses the mechanisms of the ROS production in IVDD in respect to resveratrol activity [4]. Resveratrol exerts anabolic and anti-catabolic effects by reducing the expression of inflammatory cytokines (e.g., IL-6, IL-8) and matrix metalloproteinases (e.g., MMP-3, MMP-13) and by acting indirectly on the Nrf2/Keap1/ARE pathway by inducing Nfr2 to transfer to the nucleus, therefore modulating GSH synthesis. This latter will enhance GPX1 activity that in turn will reduce lipid peroxidation products. Via AMPK/SIRT1 pathway resveratrol also regulates Mn-SOD dysfunction restoring its antioxidant enzymatic activity. Evidence also supports the involvement of miRNA in exerting the antioxidant effects. More importantly, the molecule seems to increase the proteoglycan synthesis in a dose-dependent manner, facing their pathological loss during the degeneration. The most acknowledged effect sustained by resveratrol involves the activation of SIRT1 signaling pathway which will in turn regulate and reverse ROS cytotoxicity and therefore mitochondrial dysfunction via increasing autophagic flux. Resveratrol is effective in inhibiting peroxides which represent a potential therapeutic target in IVDD. Clinical therapies based on anti-apoptotic strategies which combined resveratrol with 17 b-estradiol efficiently showed to prevent IL-1β induced apoptosis of NPCs, mainly through PI3K/AKT/mTOR/caspase-3 and PI3K/AKT/GSK-3β pathway [5,6].
Oxidative stress implications for therapeutic vaccine development against Chagas disease
Published in Expert Review of Vaccines, 2021
Subhadip Choudhuri, Lizette Rios, Juan Carlos Vázquez-Chagoyán, Nisha Jain Garg
We have tested the protective efficacy of two antigens, named TcG2 and TcG4, as immune therapy (Table 2). TcG2 and TcG4 are expressed in all mammalian stages of T. cruzi [133,134] and consist of epitopes recognized by antibodies and T cells in mice, dogs, and humans (reviewed in [99]). Further, TcG2 and TcG4 were conserved in five of the six T. cruzi lineages with 80–96% homology, thus indicating that TcG2/TcG4-based therapeutics can extend protection against various T. cruzi genotypes circulating in the USA and Latin America. In all studies, where we tested therapeutic efficacy of TcG2 and TcG4, mice were given the immune therapy in indeterminate phase when natural immune response had controlled the acute parasitemia. In the first study, C57BL/6 mice with or without overexpression of glutathione peroxidase 1 (GPx1, detoxifies ROS) were infected with T. cruzi and 45 days later given TcG2/TcG4 as a DNA-prime/protein-boost therapy [135]. All mice receiving immune therapy exhibited >15-fold reduction in blood and tissue parasites, significant reduction of chronic inflammatory infiltrate in skeletal and cardiac tissues, and of hypertrophy (BNP and ANP) and fibrosis (collagens) markers in the heart. GPx1 transgenic mice were better equipped than the wild type mice in controlling the tissue pathological responses, including markers of inflammation and fibrosis [135].
Silver nanoparticle-induced expression of proteins related to oxidative stress and neurodegeneration in an in vitro human blood-brain barrier model
Published in Nanotoxicology, 2019
Asif Manzoor Khan, Barbara Korzeniowska, Vladimir Gorshkov, Muhammad Tahir, Henrik Schrøder, Lilian Skytte, Kaare Lund Rasmussen, Surabhi Khandige, Jakob Møller-Jensen, Frank Kjeldsen
We also observed that the anti-oxidative proteins glutathione peroxidase (Gpx1) and glutathione peroxidase (Gpx4), known for their protective roles against oxidative stress, were downregulated. Expression of Gpx1 and Gpx4 has been shown to be reduced in a mouse model of AD and Parkinson disease (PD) (Zhang et al. 2016; Porcellotti et al. 2015). Studies have shown that reduced levels of Gpx1 and Gpx4 lead to neurotoxicity-mediated neurodegeneration (Zemolin et al. 2012; Yoo et al. 2010; Bellinger et al. 2011). It has also been shown that the generation of ROS leads to increased oxidative stress and that low levels of antioxidants can further exacerbate the situation (Veronesi et al. 2005). Increased AgNPs accumulation may lead to increased toxicity in cells at the initial stage, resulting in a decline of the anti-oxidant defense mechanism.