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Intracellular Redox Status and Disease Development: An Overview of the Dynamics of Metabolic Orchestra
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Sharmi Mukherjee, Anindita Chakraborty
Acyl chain lipid peroxidation due to oxidation of these lipid radicals induce the bond rearrangement of membrane phospholipids promoting further chain propagation by the capture of radicals (Hauck and Bernlohr, 2016). Depending upon the lipid species oxidized and level of unsaturation, final products like mutagenic MDA, hexanal, highly toxic 4-hydroxynonenal (4-HNE), or acrolein are produced which serve as the second messengers of oxidative stress due to their high reactivity (Barrera, 2012; Weber et al., 2013).
Interactions of Carbon Nanostructures with Lipid Membranes
Published in Heather N. Hayenga, Helim Aranda-Espinoza, Biomaterial Mechanics, 2017
There are a number of biological mechanisms proposed to explain CNT effects in biological systems. The most significant is the generation of ROS with the subsequent lipid peroxidation and development of inflammatory reactions. However, additional mechanisms could play an important role in the adverse effects of CNT, such as stated by Boczkowski and Lanone (2012):Oxidative stress is generated by the imbalance between oxidants production and antioxidants defenses. Common biomarkers of oxidative stress are malone dialdehyde (MDA), products of lipid peroxidation such as 4 hydroxynonenal (4-HNE), and protein carbonyls. The interaction with CNT causes a higher cellular inflammatory response accompanied by an increased secretion of two major inflammatory cytokenes; TNF and IL-6.Inflammation is an early event after the exposure of CNT (6–24 h) with the recruitment of neutrophil-driven infiltration accompanied by the release of protein inflammatory cytokines, tumor necrosis factor (TNF) alpha, interleukin B and 6 (IL-B, IL-6), monocyte chemo-attractant protein (MCO)-1, or macrophage inflammatory protein (MIP)-2 or CXCL-2.Genotoxic potential and mutagenic effects of CNT such as micronucleus induction, chromosome aberration and DNA damage could result as an excess of ROS and the surface properties of CNT. However, exists a controversy if CNT can play a role in genotoxic effects. Definitively, it is necessary to perform more research in order to understand CNT mechanism for genotoxic effects.Protein corona refers to the interactions between components of the biological milieu and nanoparticles. These interactions are dictated by the structural composition of the xenobiotic and mediated by surface bound proteins and lipids. All nanoparticles in biological fluids are dynamically coated with a protein/lipid mixture dependent on the size, shape, and surfaces properties of the nanoparticle. Protein corona is a major determinant of the localization and effects of nanomaterials in vivo. Protein corona in CNT could present favorable effects, for example, CNT coated with some proteins can increase their biocompatibility.Degradation, biopersistence, and systemic translocation of CNT are important issues that remain poorly characterized and understood. Enzymatic degradation by horseradish peroxidase (HRP) (Micoli et al. 2014) and myeloperoxidase (MPO) can exist in vivo and appears as a mechanism responding inflammation. However, the relevance of this phenomenon on CNT biopersistence has not been investigated yet. For example, there is no evidence of translocation between organs.
Hydroxychloroquine improves high-fat-diet-induced obesity and organ dysfunction via modulation of lipid level, oxidative stress, and inflammation
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Mohamed A Hasan, Omar A. Ammar, Maher A Amer, Azza I Othman, Fawzia Zigheber, Mohamed A El-Missiry
Serum lipid fraction levels, including total lipids, total cholesterol (TC), triglycerides (TG), and high-density lipoprotein (HDL), were assessed using colorimetric test kits purchased from Spinreact (Girona, Spain). Friedewald’s formula was used to calculate the level of low-density lipoprotein cholesterol (LDL-C) and very low-density lipoprotein cholesterol (VLDL-C) [19]. Creatine kinase myocardial band (CK-MB) and lactic dehydrogenase (LDH) activities in the serum were estimated in accordance with the standard methods using kits purchased from BioSystems (Barcelona, Spain). Serum troponin T level was determined using the sandwich enzyme immunoassay technique kit purchased from Kamiya Biomedical (Seattle, USA). Lipid peroxidation was determined by estimating the amount of 4-hydroxynonenal (4-HNE) according to the manufacturer’s instructions (FineTest, Wuhan, China). Glutathione (GSH) concentration and glutathione peroxidase (GPx) activities were estimated using kits supplied by Biodiagnostic (Giza, Egypt). Serum IL-6, IL-10, and TNF-α levels were assessed using ELISA kits purchased from BosterBio (California, USA) and ElisaGenie (London, UK). Leptin and adiponectin were measured in serum using an ELISA mouse leptin immunoassay kit (Catalog No: MOB00) and ELISA mouse Adiponectin/Acrp30 immunoassay kit (Catalog No: MRP300) obtained from R & D systems, MN, USA. Plasma D-dimer was determined using the Innovance D-dimer assay (Siemens, Marburg, Germany).
Evaluation of the Potential Impact of Medical Ozone Therapy on Covid-19: A Review Study
Published in Ozone: Science & Engineering, 2023
Furthermore, ozone produces reactive oxygen species (ROS) in the plasma, and these molecules trigger several biochemical routes and thus promote the efficacy of the ozone treatment by increasing the antioxidant enzyme levels in the plasma, which can also be evaluated as a reason for the increase of antioxidant enzyme levels (Bocci et al. 1998). Ozone reduces lipid peroxidation, edema and excitotoxic and mitochondrial injury and it also inhibits infarction by inducing the release of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-s-transferase (GSTr), catalase (CAT), heme-oxygenase-1 (HO-1), NADPH-quinone-oxidoreductase (NQO-1), phase II enzymes of drug metabolism, and heat shock proteins (HSP) (Sagai et al. 2011) (Figure 2). When ozone reaches plasma, it is decomposed and therefore it enters into a quicker reaction with antioxidants and produces polyunsaturated fatty acids (PUFA), hydrogen peroxide (H2O2) and lipid peroxidation products, and it activates physiological functions of 4-hydroxynonenal (4-HNE) on blood and endothelial cells, which play a role in the healing of several diseases (Sagai et al. 2011) (Figure 2). It is stated that H2O2 acts as the secondary messenger of ozone, and is responsible for at least some of its therapeutic effects. One of its first effects is to cause a shift of the oxygen–hemoglobin dissociation curve toward the right and thus to facilitate oxygen release in the tissues by increasing the level of 2,3-diphosphoglycerate (2,3-DPG) in erythrocytes (Sagai et al. 2011). The concentration of H2O2 increases in the plasma, and it diffuses quickly into the cells and triggers the construction of nuclear factor-kappa B (NF-κB), NO-synthase and protein kinases, increasing the synthesis and release of TNFα, IL-1, IL-8, IFNγ and TGFβ1 via ozone treatment (Sagai et al. 2011). Both metabolic (hexose monophosphate shunt) and immunological (via the transcription factor NF-kB) mechanisms are stimulated by the formation of H2O2. It can be concluded that while immunosuppressants and ozone have efficacy in suppressing inflammation, it is possible that a synergistic mechanism could be triggered among immunosuppressants and ozone, resulting in a total anti-inflammatory outcome that is greater than the sum of individual potencies of these methods. Such potential benefit of adding ozone on top of the immunosuppressant regimen might aid in achieving the same anti-inflammatory efficacy to prevent the hyperinflammation syndrome, albeit with lower levels of immunosuppressants, which could possibly enable more desirable side effect profiles.