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 F2α (8-iso-PGF2α) 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-PGF2α 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-PGF2α levels by g = 0.38 ± 0.04; therefore, the overall reduction of 8-iso-PGF2α levels is ≈ 90% by this treatment in this specific medical condition. In conclusion, 8-iso-PGF2α levels can be reduced not only by antioxidants but by many other strategies. Not all strategies are equally effective at reducing 8-iso-PGF2α levels. In addition, the effectiveness of any strategy can be assessed only in relation to the medical condition investigated.
journal_name
Redox Bioljournal_title
Redox biologyauthors
van 't Erve TJdoi
10.1016/j.redox.2018.05.003subject
Has Abstractpub_date
2018-07-01 00:00:00pages
284-296issn
2213-2317pii
S2213-2317(18)30296-9journal_volume
17pub_type
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