Plasma Non-Enzymatic Antioxidant Capacity (NEAC) in Relation to Dietary NEAC, Nutrient Antioxidants and Inflammation-Related Biomarkers.

María-José Sánchez,Cayetano Javier Carrión-García,Pilar Amiano,Eduardo Jesús Guerra-Hernández,Belén García-Villanova,Esther Molina-Montes,Mauro Serafini

doi:10.3390/antiox9040301

Abstract

(1) Background: Little is known about the interlinkages between dietary and plasma non-enzymatic antioxidant capacity (D-NEAC and P-NEAC, respectively) and the body’s antioxidant and inflammation response. Our aim was to explore these associations in 210 participants from two Spanish European Prospective Investigation into Cancer and Nutrition (EPIC) centers. (2) Methods: D-NEAC was estimated using published NEAC values in food. P-NEAC and total polyphenols (TP) were quantified by FRAP (ferric-reducing antioxidant power), TRAP (total radical-trapping antioxidant parameter), TEAC-ABTS (trolox equivalent antioxidant capacity-Azino Bis Thiazoline Sulfonic), ORAC (oxygen radical absorbance capacity) and Folin–Ciocalteu assays. Nutrient antioxidants (carotenes, α-tocopherol, ascorbic acid, retinol, uric acid, Q9 and Q10 coenzymes) and inflammation markers (IL-6, IL-8, CRP, TNF-α, PAI-I, resistin and adiponectin) were also analyzed. Spearman correlation and linear regression analyses were performed in association analyses. Analyses were stratified by covariates and groups were defined using cluster analysis. (3) Results: P-FRAP was correlated with D-NEAC, and significantly associated with P-NEAC in multivariate adjusted models. P-FRAP levels were also significantly associated with plasma antioxidants (log2 scale: TP β = 0.26; ascorbic acid β = 0.03; retinol β = 0.08; α-tocopherol β = 0.05; carotenes β = 0.02; Q10 β = 0.06; uric acid β = 0.25), though not with inflammation-related biomarkers. Different profiles of individuals with varying levels of P-NEAC and biomarkers were found. (4) Conclusions: P-NEAC levels were to some extent associated with D-NEAC and plasma antioxidants, yet not associated with inflammation response.

Highlights

IntroductionAn increased production of free radicals and reactive oxygen species (ROS) arise from a variety of sources (endogenous metabolic reactions and exogenous factors, e.g., pollution, smoke or UV irradiation), but living organisms have developed protection mechanisms against oxidative stress (OS) [1,2]
An increased production of free radicals and reactive oxygen species (ROS) arise from a variety of sources, but living organisms have developed protection mechanisms against oxidative stress (OS) [1,2]
By center (Table S1), there was a higher proportion of women in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Granada center (p-value < 0.001), and a higher rate of non-formal education, of people who had never smoked and of physically inactive individuals (p-value < 0.001)

Summary

Introduction

An increased production of free radicals and reactive oxygen species (ROS) arise from a variety of sources (endogenous metabolic reactions and exogenous factors, e.g., pollution, smoke or UV irradiation), but living organisms have developed protection mechanisms against oxidative stress (OS) [1,2]. The main mechanism comprises the endogenous enzymatic antioxidant system, but dietary non-enzymatic antioxidants are essential to counteract this process as well. Fruits and vegetables are the main sources of dietary antioxidants including vitamin C, vitamin E and carotenoids [1]. These compounds protect cells from free radical-induced oxidative damage [2,3,4], thereby contributing to reducing the risk of several non-communicable chronic diseases and aging. The main NEAC assays are oxygen radical absorbance capacity (ORAC), total radical-trapping antioxidant parameter (TRAP), trolox equivalent antioxidant capacity-Azino Bis Thiazoline Sulfonic (TEAC-ABTS) and ferric-reducing antioxidant power (FRAP) [5]

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