Use of conventional and -omics based methods for health claims of dietary antioxidants: a critical overview

Abstract

This article describes the principles and limitations of methods used to investigate reactive oxygen species (ROS) protective properties of dietary constituents and is aimed at providing a better understanding of the requirements for science based health claims of antioxidant (AO) effects of foods. A number of currently used biochemical measurements aimed of determining the total antioxidant capacity and oxidised lipids and proteins are carried out under unphysiologcial conditions and are prone to artefact formation. Probably the most reliable approaches are measurements of isoprostanes as a parameter of lipid peroxidation and determination of oxidative DNA damage. Also the design of the experimental models has a strong impact on the reliability of AO studies: the common strategy is the identification of AO by in vitro screening with cell lines. This approach is based on the assumption that protection towards ROS is due to scavenging, but recent findings indicate that activation of transcription factors which regulate genes involved in antioxidant defence plays a key role in the mode of action of AO. These processes are not adequately represented in cell lines. Another shortcoming of in vitro experiments is that AO are metabolised in vivo and that most cell lines are lacking enzymes which catalyse these reactions. Compounds with large molecular configurations (chlorophylls, anthocyans and polyphenolics) are potent AO in vitro, but weak or no effects were observed in animal/human studies with realistic doses as they are poorly absorbed. The development of -omics approaches will improve the scientific basis for health claims. The evaluation of results from microarray and proteomics studies shows that it is not possible to establish a general signature of alterations of transcription and protein patterns by AO. However, it was shown that alterations of gene expression and protein levels caused by experimentally induced oxidative stress and ROS related diseases can be normalised by dietary AO.

The Role of Biomarkers of Oxidative Stress in Breast Cancer Risk and Prognosis: A Systematic Review of the Epidemiologic Literature

“…7,[15][16][17][18][19][20][21] Commonly used biomarkers include DNA damage biomarkers, such as 8-hydroxy-2¢-deoxyguanosine (8-oxodG), 22 protein carbonyl groups as a marker of protein oxidation, 23 and malondialdehyde (MDA) and F2-isoprostanes as markers of lipid peroxidation. 21,[24][25][26][27] Studies have also evaluated the role of oxidative stress in cancer and other chronic diseases using plasma fluorescent oxidation products (FlOPs), which are considered a global biomarker of oxidative stress. 20,28 Biomarkers of oxidative stress have been investigated for their association with the development and progression of several cancer types, and in particular breast cancer, as oxidative stress mechanisms may be involved in several known breast cancer risk factors, including obesity and daily alcohol intake, and circulating estrogen levels.…”

Scientific Opinion Part I on the substantiation of health claims related to various food(s)/food constituent(s) not supported by pertinent human data (ID 411, 559, 1174, 1184, 1197, 1380, 1409, 1656, 1667, 1670, 1763, 1767, 1806, 1884, 1908, 1997, 2141, 2

“…These methods included total reactive antioxidant potential (TRAP), trolox-equivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC), and dichlorofluorescein (DCF) fluorescence. The Panel considers that the evidence provided in these studies does not predict the occurrence of an effect of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage (Dalle-Donne et al, 2006;Griffiths et al, 2002;Knasmuller et al, 2008;Mayne, 2003).…”

“…Such markers are thiobarbituric acid-reactive substances (TBARS), malondialdehyde (MDA) and/or oxidation lag time of LDL ex vivo and/or autoantibodies against oxidised LDL particles. The Panel considers that both TBARS and MDA, when used alone, are not reliable markers of lipid peroxidation (Griffiths et al, 2002;Knasmuller et al, 2008;Lykkesfeldt, 2007). The Panel also considers that no evidence has been provided to establish that the oxidation lag time of LDL particles ex vivo or that autoantibodies against oxidised LDL particles predict the resistance of LDL particles to peroxidation in vivo (Griffiths et al, 2002;Lapointe et al, 2006;Verhoye and Langlois, 2009).…”

Scientific Opinion on the substantiation of health claims related to various food(s)/food constituent(s) and protection of cells from premature ageing (ID 1668, 1917, 2515, 2527, 2530, 2575, 2580, 2591, 2620, 3178, 3179, 3180, 3181, 4329, 4415), antioxida

“…These methods include total reactive antioxidant potential (TRAP), troloxequivalent antioxidant capacity (TEAC), ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC) and ferrous oxidation-xylenol orange (FOX). The Panel considers that the evidence provided in these studies does not predict the occurrence of an effect of the consumption of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage (Griffiths et al, 2002;Mayne, 2003;Dalle-Donne, et al, 2006;Knasmuller et al, 2008). A number of intervention studies assessed changes in antioxidant enzymes (e.g.…”