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      Oxidative Stress and Preterm Birth: An Integrative Review

      1 , 2 , 3
      Biological Research For Nursing
      SAGE Publications

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          Abstract

          <div class="section"> <a class="named-anchor" id="d1045281e137"> <!-- named anchor --> </a> <h5 class="section-title" id="d1045281e138">Background:</h5> <p id="d1045281e140">A variety of methods and measures have been used to quantify oxidative stress in clinical studies related to preterm birth (PTB), and studies have reported conflicting findings. No integrative reviews have been conducted. </p> </div><div class="section"> <a class="named-anchor" id="d1045281e142"> <!-- named anchor --> </a> <h5 class="section-title" id="d1045281e143">Objective:</h5> <p id="d1045281e145">To describe specific molecules used as markers of oxidative stress and methods to measure these molecules and to review the literature for associations between oxidative stress and PTB specific to these molecules. </p> </div><div class="section"> <a class="named-anchor" id="d1045281e147"> <!-- named anchor --> </a> <h5 class="section-title" id="d1045281e148">Method:</h5> <p id="d1045281e150">Systematic literature searches were conducted in June 2015 and updated in 2017 in databases from the <i>Biomedical Reference Collection: Basic Edition</i>, including MEDLINE and <a data-untrusted="" href="http://clinicaltrials.gov" id="d1045281e155" target="xrefwindow">clinicaltrials.gov</a>. Articles were included if they described original research published after 2009 and compared PTB or preterm premature rupture of membranes with term birth (TB). </p> </div><div class="section"> <a class="named-anchor" id="d1045281e158"> <!-- named anchor --> </a> <h5 class="section-title" id="d1045281e159">Results:</h5> <p id="d1045281e161">Abstracts ( <i>n</i> = 3,107) were reviewed for inclusion/exclusion criteria. Of these, 308 were full-text reviewed, and 30 articles were included in this review. All were identified as nonexperimental. The most common measurements of oxidative stress were quantification of total oxidant or antioxidant status or lipid peroxidation. Studies measuring reactive oxygen species or by-products of oxidative stress reported higher levels of these molecules for preterm specimens compared to TB specimens. Studies measuring antioxidants reported lower levels for these molecules in PTB specimens. Few of the studies had inconclusive findings. </p> </div><div class="section"> <a class="named-anchor" id="d1045281e166"> <!-- named anchor --> </a> <h5 class="section-title" id="d1045281e167">Discussion:</h5> <p id="d1045281e169">Findings suggest that an imbalance between oxidants and antioxidants may be associated with PTB. The measurements and findings to date limit interpretation and understanding. Research using multidimensional methods and multidisciplinary teams are necessary to advance research and practice. </p> </div>

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          The role of antioxidants in the chemistry of oxidative stress: A review.

          This Review Article is focused on the action of the reactive oxygenated species in inducing oxidative injury of the lipid membrane components, as well as on the ability of antioxidants (of different structures and sources, and following different mechanisms of action) in fighting against oxidative stress. Oxidative stress is defined as an excessive production of reactive oxygenated species that cannot be counteracted by the action of antioxidants, but also as a perturbation of cell redox balance. Reactive oxygenated/nitrogenated species are represented by superoxide anion radical, hydroxyl, alkoxyl and lipid peroxyl radicals, nitric oxide and peroxynitrite. Oxidative stress determines structure modifications and function modulation in nucleic acids, lipids and proteins. Oxidative degradation of lipids yields malondialdehyde and 4-hydroxynonenal, but also isoprostanes, from unsaturated fatty acids. Protein damage may occur with thiol oxidation, carbonylation, side-chain oxidation, fragmentation, unfolding and misfolding, resulting activity loss. 8-hydroxydeoxyguanosine is an index of DNA damage. The involvement of the reactive oxygenated/nitrogenated species in disease occurrence is described. The unbalance between the oxidant species and the antioxidant defense system may trigger specific factors responsible for oxidative damage in the cell: over-expression of oncogene genes, generation of mutagen compounds, promotion of atherogenic activity, senile plaque occurrence or inflammation. This leads to cancer, neurodegeneration, cardiovascular diseases, diabetes, kidney diseases. The concept of antioxidant is defined, along with a discussion of the existent classification criteria: enzymatic and non-enzymatic, preventative or repair-systems, endogenous and exogenous, primary and secondary, hydrosoluble and liposoluble, natural or synthetic. Primary antioxidants are mainly chain breakers, able to scavenge radical species by hydrogen donation. Secondary antioxidants are singlet oxygen quenchers, peroxide decomposers, metal chelators, oxidative enzyme inhibitors or UV radiation absorbers. The specific mechanism of action of the most important representatives of each antioxidant class (endogenous and exogenous) in preventing or inhibiting particular factors leading to oxidative injury in the cell, is then reviewed. Mutual influences, including synergistic effects are presented and discussed. Prooxidative influences likely to occur, as for instance in the presence of transition metal ions, are also reminded.
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            The Haber-Weiss reaction and mechanisms of toxicity.

            The concept that the highly reactive hydroxyl radical (HO) could be generated from an interaction between superoxide (O(2)(-)) and hydrogen peroxide (H(2)O(2)) was proposed (with Joseph Weiss) in Professor Haber's final paper published in 1934. Until it was recognized that free radicals are produced in biological systems, this finding seemed to have no relevance to biology. However, following the discovery that O(2)(-) was a normal cellular metabolite, it was quickly recognized that the Haber-Weiss reaction (O(2)(-)+H(2)O(2) -->HO+O(2)+HO(-)) might provide a means to generate more toxic radicals. Although the basic reaction has a second order rate constant of zero in aqueous solution and thus cannot occur in biological systems, the ability of iron salts to serve as catalysts was discussed by these authors. Because transition metal ions, particularly iron, are present at low levels in biological systems, this pathway (commonly referred to as the iron-catalyzed Haber-Weiss reaction) has been widely postulated to account for the in vivo generation of the highly reactive HO. Recent data documenting the importance of redox regulation of various cellular signaling pathways makes it clear that free radicals are essential for normal cellular function. However, this also makes it obvious that disruptions of free radical production or defenses at many different levels can lead to adverse effects on cells. While the generation of HO, which is by far the most reactive oxygen species, is generally indicative of an overtly toxic event, it is through studies at this level that we have reached a better understanding of free radicals as both signaling molecules and toxic species.
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              Carotenoids, inflammation, and oxidative stress--implications of cellular signaling pathways and relation to chronic disease prevention.

              Several epidemiologic studies have shown that diets rich in fruits and vegetables reduce the risk of developing several chronic diseases, such as type 2 diabetes, atherosclerosis, and cancer. These diseases are linked with systemic, low-grade chronic inflammation. Although controversy persists on the bioactive ingredients, several secondary plant metabolites have been associated with these beneficial health effects. Carotenoids represent the most abundant lipid-soluble phytochemicals, and in vitro and in vivo studies have suggested that they have antioxidant, antiapoptotic, and anti-inflammatory properties. Recently, many of these properties have been linked to the effect of carotenoids on intracellular signaling cascades, thereby influencing gene expression and protein translation. By blocking the translocation of nuclear factor κB to the nucleus, carotenoids are able to interact with the nuclear factor κB pathway and thus inhibit the downstream production of inflammatory cytokines, such as interleukin-8 or prostaglandin E2. Carotenoids can also block oxidative stress by interacting with the nuclear factor erythroid 2-related factor 2 pathway, enhancing its translocation into the nucleus, and activating phase II enzymes and antioxidants, such as glutathione-S-transferases. In this review, which is organized into in vitro, animal, and human investigations, we summarized current knowledge on carotenoids and metabolites with respect to their ability to modulate inflammatory and oxidative stress pathways and discuss potential dose-health relations. Although many pathways involved in the bioactivity of carotenoids have been revealed, future research should be directed toward dose-response relations of carotenoids, their metabolites, and their effect on transcription factors and metabolism.
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                Author and article information

                Journal
                Biological Research For Nursing
                Biological Research For Nursing
                SAGE Publications
                1099-8004
                1552-4175
                August 02 2018
                October 2018
                August 2018
                October 2018
                : 20
                : 5
                : 497-512
                Affiliations
                [1 ]College of Nursing, University of Nebraska Medical Center, Omaha, NE, USA
                [2 ]College of Allied Health Professions, University of Nebraska Medical Center, Omaha, NE, USA
                [3 ]College of Medicine, University of Nebraska Medical Center, Omaha, NE, USA
                Article
                10.1177/1099800418791028
                6346316
                30068228
                2541daaa-d422-4ca9-968d-ba42b7b293db
                © 2018

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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