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A potential contributing factor in the development of various metabolic diseases such as nonalcoholic fatty liver disease (NAFLD) could be oxidative stress and the production of reactive oxygen radicals. A high level of lipid peroxidation, including oxidative stress, can cause irreversible effects. We investigated the consequences of NAFLD on the reducing power of the liver in patients through plasma antioxidant capacity using screen‐printed electrodes (SPEs). The study includes a total of 67 patient’s population with steatosis ( n = 29) and steatohepatitis ( n = 38). Anodic current intensity ( la ), anodic wave area ( S ), and the biological sample oxidation potentials can be determined via cyclic voltammetry (CV) analysis. The enzyme glutathione peroxidase (GPx) and products of oxidative damage such as malondialdehyde (MDA), advanced glycation‐end product (AGE), total status of oxidants (TOS), nitric oxide (NO), and cytokines analysis (qRT‐PCR) of key mediators such as PNPLA3 in lipid metabolism, TIMP1 in fibrosis, and proinflammatory cytokines like NF‐ κ B, TNF‐ α , and IL‐6, which are crucial for understanding NAFLD progression were recorded to further validate the CV obtained results along with and morphological changes through scanning electron microscope (SEM). The developed method measured oxidative stress with an error of less than 1.3% in human plasma samples, wherein the steatohepatitis caused a spike modification in the anodic current AC 520 and AC 972 ( p < 0.01) compared to healthy humans. The presented electroanalytical methodology could be widely used for easy and rapid subjects’ disease status detection. In addition to monitoring the response of subjects to treatment and providing nutritional supplements, these results may also be used for screening specific populations.

Oxidative stress is an important mechanism for the development and progression of chronic obstructive pulmonary disease (COPD). It may also contribute to systemic manifestation in patients with COPD. Reactive oxygen species (ROS) including free radicals play a crucial role in oxidative stress in COPD. The aims of this study were to determine serum scavenging capacity profile against multiple free radicals and to evaluate its correlation with pathophysiology, exacerbations, and prognosis in patients with COPD. Serum scavenging capacity profile against multiple free radicals comprising hydroxyl radical ( OH), superoxide radical (O ), alkoxy radical (RO ), methyl radical ( CH ), alkylperoxyl radical (ROO ), and singlet oxygen ( O ) was assessed using the multiple free-radical scavenging method in 37 patients with COPD (mean age, 71 years; mean forced expiratory volume in 1 s, 55.2% predicted). The severity of emphysema was evaluated by Goddard classification on chest computed tomography. Exacerbations were recorded prospectively for 1 year and the overall mortality was assessed 5 years after the initial assessment. OH scavenging capacity was significantly decreased (p < 0.05) and O and CH scavenging capacity tended to decrease in patients with COPD compared to that in healthy controls. On the other hand, ROO scavenging capacity tended to increase. In addition, RO scavenging capacity was associated with severity of emphysema (p < 0.05) and exacerbation frequency (p < 0.02). There was a difference in the profile of the scavenging capacity between survived and deceased patients with COPD for 5 years after initial assessment. Characteristic profile of free radical scavenging capacity can provide insight into the pathophysiology and prognosis of patients with COPD.

Oxidative stress is associated with asthma pathobiology. We reported that oxidized phosphatidylcholines (OxPCs) are mediators of oxidative stress and accumulate in the lung in response to allergen challenge. The current study begins to unravel mechanisms for OxPC accumulation in the lung, providing the first insights about how OxPCs underpin allergic airway pathophysiology, and pre-clinical testing of selective neutralization of OxPCs in a murine model of allergic asthma. We hypothesized that intranasal delivery of E06, a natural IgM antibody that neutralizes the biological activity of OxPCs, can ameliorate allergen-induced airway inflammation and airway hyperresponsiveness. Adult BALB/c mice were intranasally (i.n.) challenged with house dust mite (HDM) (25 μg/mouse, 2 weeks). Some animals also received E06 monoclonal antibody (mAb) (10 µg) i.n. 1 hr before each HDM challenge. HDM challenge reduced mRNA for anti-oxidant genes (SOD1, SOD2, HO-1, and NFE2L2) in the lung by several orders of magnitude (p < 0.05). Concomitantly, total immune cell number in bronchoalveolar lavage fluid (BALF) increased significantly (p < 0.001). E06 mAb treatment prevented allergen-induced BALF immune cell number by 43% (p < 0.01). This included a significant blockade of eosinophils (by 48%, p < 0.001), neutrophils (by 80%, p < 0.001), macrophages (by 80%, p < 0.05), and CD4 (by 30%, p < 0.05) and CD8 (by 42%, p < 0.01) lymphocytes. E06 effects correlated with a significant reduction in TNF (by 64%, p < 0.001) and IL-1β (by 75%, p < 0.05) and a trend to diminish accumulation of other cytokines (e.g., IL-4, -10, and -33, and IFN-γ). E06 mAb treatment also inhibited HDM exposure-induced increases in total respiratory resistance and small airway resistance by 24% and 26%, respectively. In conclusion, prophylactic treatment with an OxPC-neutralizing antibody significantly limits allergen-induced airway inflammation and airway hyperresponsiveness, suggesting that OxPCs are important mediators of oxidative stress-associated allergic lung pathophysiology.

This publication contains an extensive overview of free radicals and diseases, including both basic science approaches and clinical applications. The research of the last decades has contributed substantially to the understanding role and function of these metabolites. It is the aim of the editors to include a large variety of biological models ranging from yeast over mitochondria, isolated cells and cell culture models to animals and humans. The topics discussed focus on the function and integrity of mitochondria under oxidative conditions, the role of protein oxidation and proteolysis in the cellular stress response. Also the new aspects in the fields of antioxidant treatment are dealt with intensively. Some chapters introduce more methodological approaches and their application in the investigation of oxidative stress and diseases related to this condition.

This volume contains contributions by some of the leading scientists in the field of thiol oxidation/reduction (redox) biochemistry. It is focused on the biological/pathophysiological implications of newly-discovered functions of cellular thiols, such as glutathione in the first place.

We compared the effects of dextrans with a molecular weight of 35 kDa oxidized by chemical (OD ch ) and radiochemical (OD r ) methods on oxidative and metabolic functions of peritoneal macrophages from BALB/c mice in vitro and in vivo . It was found that none type of dextrans exhibits chemiluminescent properties. In vitro study showed that OD ch had a priming effect on mouse peritoneal macrophages, while OD r did not potentiate the oxidative and metabolic response of cells to zymosan. Being injected intraperitoneally, OD r more markedly enhanced chemiluminescent response of mouse peritoneal macrophages and reduced their viability than OD ch . Thus, both dextrans are biocompatible, but in OD ch this parameter is higher.

The red tide organism Heterosigma akashiwo (Raphidophyceae) has been associated with rapid death of fish for many years. The precise toxicological mechanism(s) involved in these fish kills is unclear. Proposed mechanisms of toxicity include the production of reactive oxygen species (ROS), the release of large quantities of mucus from mucocysts, and/or the production of an organic toxin. Initially, I investigated the potential of H. akashiwo to produce extracellular hydrogen peroxide (H2O2) and investigated which cellular processes were responsible for this production. I determined that production of extracellular H2O2 by H. akashiwo occurs through a metabolic pathway that is not directly linked to photosynthesis. Within all experiments, different isolates of H. akashiwo produced variable levels of H2O2 amounting to extracellular concentrations of up to 0.5 μM. However, lethality experiments indicated that production of H2O2 by isolates of H. akashiwo is orders of magnitude less than that required for mortality of either vertebrate cell lines or invertebrate Artemia saliva. To consider alternative modes of toxicity, I collected and tested the bioactivity of extracellular organics from multiple H. akashiwo cultures on cellular activity and viability in mammalian cells, and cytosolic calcium levels (Ca 2+i) in Sf9 insect cells. Cellular activity of the mammalian cells, as assessed by mitochondrial dehydrogenase activity, increased up to 15-fold, depending on length of exposure and concentration of the extracellular organics. Moreover, there was a dichotomy between cultured isolates of H. akashiwo, those that produce the bioactive organic, and those isolates that did not. Cytosolic calcium is a signalling second messenger in all organisms that controls many facets of cellular activity. In real-time, exposure of the organics elevated Ca2+i in a concentration-dependent manner up to 125 nM above basal (2-fold elevation). Cytosolic Ca2+ stimulation rapidly peaked, followed by a sustained plateau. Collectively, the data indicate that a bioactive compound(s) from specific cultures of H. akashiwo can alter cellular activity and induce apoptosis in mammalian cells, and inhibit the plasma membrane Ca2+-ATPase transporter in Sf9 cells. I propose that this bioactive organic(s) may have significant ecological impacts on algal succession, allelopathy and/or fish kills.