16
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Strategies to decrease oxidative stress biomarker levels in human medical conditions: A meta-analysis on 8-iso-prostaglandin F

      research-article
      a , b , *
      Redox Biology
      Elsevier

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The widespread detection of elevated oxidative stress levels in many medical conditions has led to numerous efforts to design interventions to reduce its effects. Efforts have been wide-ranging, from dietary changes to administration of antioxidants, supplements, e.g., omega-3-fatty acids, and many medications. However, there is still no systemic assessment of the efficacy of treatments for oxidative stress reduction across a variety of medical conditions.

          The goal of this meta-analysis is, by combining multiple studies, to quantitate the change in the levels of the popular oxidative stress biomarker 8-iso-prostaglandin F (8-iso-PGF ) after a variety of treatment strategies in human populations.

          Nearly 350 unique publications with 180 distinct strategies were included in the analysis. For each strategy, the difference between pre- or placebo and post-treatment levels calculated using Hedges’ g value of effect. In general, administration of antibiotics, antihyperlipidemic agents, or changes in lifestyle (g = − 0.63, − 0.54, and 0.56) had the largest effect. Administration of supplements, antioxidants, or changes in diet (g = − 0.09, − 0.28, − 0.12) had small quantitative effects. To fully interpret the effectiveness of these treatments, comparisons to the increase in g value for each medical condition is required. For example, antioxidants in populations with coronary artery disease (CAD) reduce the 8-iso-PGF levels by g = − 0.34 ± 0.1, which is quantitatively considered a small effect. However, CAD populations, in comparison to healthy populations, have an increase in 8-iso-PGF levels by g = 0.38 ± 0.04; therefore, the overall reduction of 8-iso-PGF levels is ≈ 90% by this treatment in this specific medical condition.

          In conclusion, 8-iso-PGF levels can be reduced not only by antioxidants but by many other strategies. Not all strategies are equally effective at reducing 8-iso-PGF levels. In addition, the effectiveness of any strategy can be assessed only in relation to the medical condition investigated.

          Highlights

          • Many strategies beyond traditional antioxidants reduce 8-iso-PGF .

          • The effectiveness of each strategy is dependent on the medical condition.

          • General statements on the effectiveness of strategies should be avoided.

          Graphical abstract

          Related collections

          Most cited references323

          • Record: found
          • Abstract: found
          • Article: not found

          Tea catechins and polyphenols: health effects, metabolism, and antioxidant functions.

          Increasing interest in the health benefits of tea has led to the inclusion of tea extracts in dietary supplements and functional foods. However, epidemiologic evidence regarding the effects of tea consumption on cancer and cardiovascular disease risk is conflicting. While tea contains a number of bioactive chemicals, it is particularly rich in catechins, of which epigallocatechin gallate (EGCG) is the most abundant. Catechins and their derivatives are thought to contribute to the beneficial effects ascribed to tea. Tea catechins and polyphenols are effective scavengers of reactive oxygen species in vitro and may also function indirectly as antioxidants through their effects on transcription factors and enzyme activities. The fact that catechins are rapidly and extensively metabolized emphasizes the importance of demonstrating their antioxidant activity in vivo. In humans, modest transient increases in plasma antioxidant capacity have been demonstrated following the consumption of tea and green tea catechins. The effects of tea and green tea catechins on biomarkers of oxidative stress, especially oxidative DNA damage, appear very promising in animal models, but data on biomarkers of in vivo oxidative stress in humans are limited. Larger human studies examining the effects of tea and tea catechin intake on biomarkers of oxidative damage to lipids, proteins, and DNA are needed.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            How do nutritional antioxidants really work: nucleophilic tone and para-hormesis versus free radical scavenging in vivo.

            We present arguments for an evolution in our understanding of how antioxidants in fruits and vegetables exert their health-protective effects. There is much epidemiological evidence for disease prevention by dietary antioxidants and chemical evidence that such compounds react in one-electron reactions with free radicals in vitro. Nonetheless, kinetic constraints indicate that in vivo scavenging of radicals is ineffective in antioxidant defense. Instead, enzymatic removal of nonradical electrophiles, such as hydroperoxides, in two-electron redox reactions is the major antioxidant mechanism. Furthermore, we propose that a major mechanism of action for nutritional antioxidants is the paradoxical oxidative activation of the Nrf2 (NF-E2-related factor 2) signaling pathway, which maintains protective oxidoreductases and their nucleophilic substrates. This maintenance of "nucleophilic tone," by a mechanism that can be called "para-hormesis," provides a means for regulating physiological nontoxic concentrations of the nonradical oxidant electrophiles that boost antioxidant enzymes, and damage removal and repair systems (for proteins, lipids, and DNA), at the optimal levels consistent with good health.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

              It has been hypothesized that the pathogenesis of diseases induced by cigarette smoking involves oxidative damage by free radicals. However, definitive evidence that smoking causes the oxidative modification of target molecules in vivo is lacking. We conducted a study to determine whether the production of F2-isoprostanes, which are novel products of lipid peroxidation, is enhanced in persons who smoke. We measured the levels of free F2-isoprostanes in plasma, the levels of F2-isoprostanes esterified to plasma lipids, and the urinary excretion of metabolites of F2-isoprostanes in 10 smokers and 10 nonsmokers matched for age and sex. The short-term effects of smoking (three cigarettes smoked over 30 minutes) and the effects of two weeks of abstinence from smoking on levels of F2-isoprostanes in the circulation were also determined in the smokers. Plasma levels of free and esterified F2-isoprostanes were significantly higher in the smokers (242 +/- 147 and 574 +/- 217 pmol per liter, respectively) than in the nonsmokers (103 +/- 19 and 345 +/- 65 pmol per liter; P = 0.02 for free F2-isoprostanes and P = 0.03 for esterified F2-isoprostanes). Smoking had no short-term effects on the circulating levels of F2-isoprostanes. However, the levels of free and esterified F2-isoprostanes fell significantly after two weeks of abstinence from smoking (250 +/- 156 and 624 +/- 214 pmol per liter, respectively, before the cessation of smoking, as compared with 156 +/- 67 and 469 +/- 108 pmol per liter after two weeks' cessation; P = 0.03 for free F2-isoprostanes and P = 0.02 for esterified F2-isoprostanes). The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.
                Bookmark

                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                09 May 2018
                July 2018
                09 May 2018
                : 17
                : 284-296
                Affiliations
                [a ]Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA
                [b ]Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA
                Author notes
                [* ]Correspondence address: Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, 27709 NC, USA. thomas.vanterve@ 123456nih.gov
                Article
                S2213-2317(18)30296-9
                10.1016/j.redox.2018.05.003
                6007822
                29775960
                7353b5f2-09e0-4fe9-8f4a-5f6da77c2b34

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 12 April 2018
                : 7 May 2018
                : 8 May 2018
                Categories
                Research Paper

                Comments

                Comment on this article