1.3. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1200, 1229, 1243, 1256, 1257, 1258, 1260, 1264, 1321, 1367, 1439, 1445, 1679, 1706, 1867, 1878, 1880, 1921, 1934, 1940, 1941, 1957, 1966, 1999, 2025, 2043, 2059, 2061, 2083, 2087, 2090, 2125, 2136, 2144, 2151, 2154, 2156, 2181, 2188, 2193, 2263, 2321, 2511, 2641, 2653, 2654, 2668, 2734, 2795, 2835, 2849, 2854, 2857, 3166, 3167, 3168, 3169, 3174, 3175, 3176, 3177, 3183, 3200, 3212, 3216, 3232, 3241, 3256, 3269, 3277, 3290, 3297, 3299, 3307, 3315, 3316, 3337, 3349, 3353, 3356, 3362, 3374, 3383, 3386, 3400, 3406, 3409, 3412, 3418, 3423, 3437, 3444, 3448, 3454, 3456, 3460, 3469, 3484, 3485, 3494, 3505, 3507, 3520, 3524, 3541, 3549, 3571, 3593, 3597, 3606, 3646, 3652, 3662, 3678, 3679, 3701, 3705, 3712, 3729, 3767, 3780, 3786, 3790, 3797, 3800, 3813, 3815, 3816, 3817, 3822, 3824, 3825, 3828, 3836, 3838, 3839, 3849, 3854, 3856, 3888, 3899, 3916, 4007, 4150, 4163)

The claimed effects refer to the protection of body cells and molecules (such as DNA, proteins and lipids) from oxidative damage, including UV-induced oxidative damage. The Panel assumes that the target population is the general population. Reactive oxygen species (ROS) including several kinds of radicals are generated in biochemical processes (e.g. respiratory chain) and as a consequence of exposure to exogenous factors (e.g. radiation, pollutants). These reactive intermediates can damage molecules such as DNA, proteins and lipids if they are not intercepted by the antioxidant network which includes free radical scavengers like antioxidant nutrients. The Panel considers that the protection of body cells and molecules such as DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.

2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1200, 1229, 1243, 1256, 1257, 1258, 1260, 1264, 1321, 1367, 1439, 1445, 1679, 1706, 1867, 1878, 1880, 1921, 1934, 1940, 1941, 1957, 1966, 1999, 2025, 2043, 2059, 2061, 2083, 2087, 2090, 2125, 2136, 2144, 2151, 2154, 2156, 2181, 2188, 2193, 2263, 2321, 2511, 2641, 2653, 2654, 2668, 2734, 2795, 2835, 2849, 2854, 2857, 3166, 3167, 3168, 3169, 3174, 3175, 3176, 3177, 3183, 3200, 3212, 3216, 3232, 3241, 3256, 3269, 3277, 3290, 3297, 3299, 3307, 3315, 3316, 3337, 3349, 3353, 3356, 3362, 3374, 3383, 3386, 3400, 3406, 3409, 3412, 3418, 3423, 3437, 3444, 3448, 3454, 3456, 3460, 3469, 3484, 3485, 3494, 3505, 3507, 3520, 3524, 3541, 3549, 3571, 3593, 3597, 3606, 3646, 3652, 3662, 3678, 3679, 3701, 3705, 3712, 3729, 3767, 3780, 3786, 3790, 3797, 3800, 3813, 3815, 3816, 3817, 3822, 3824, 3825, 3828, 3836, 3838, 3839, 3849, 3854, 3856, 3888, 3899, 3916, 4007, 4150, 4163)

Most of the references provided addressed potential health effects of dietary antioxidants in general, or of food/food constituents other than those for which the specific claims are proposed, and/or claimed effects other than the protection of body cells and molecules from oxidative damage. The latter includes references on the development or progression of acute or chronic diseases presumed to be associated with increased levels of oxidative stress (e.g. immune dysfunction/susceptibility to infections, cardiovascular diseases, cancer, and degenerative diseases, among others) where oxidative damage to cells or molecules has not been considered as an outcome. The Panel considers that no scientific conclusions can be drawn from these references for the substantiation of the claimed effect. No human studies which investigated the effects of the food(s)/food constituent(s) on reliable markers of oxidative damage to body cells or to molecules such as DNA, proteins and lipids have been provided in relation to any of the health claims evaluated in this opinion.
Some intervention studies in humans which investigated the effects of the food(s)/food constituent(s) on the overall antioxidant capacity of plasma assessed by different methods have been provided.
Food(s)/food constituent(s) with antioxidant properties
EFSA Journal 2010; 8(2):1489 7
These methods include total reactive antioxidant potential (TRAP), trolox-equivalent 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 food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage (Griffiths et al., 2002; Mayne, 2003; Dolle-Donne, et al., 2006; Knasmuller et al., 2008). Some intervention studies in humans having investigated the effects of the food(s)/ food constituent(s) on markers of lipid peroxidation have been provided in relation to ID 1243, 1468, 1850, 2060, 2511, 2835, 3505 and 3678. Such markers are thiobarbituric acid-reactive substances (TBARS), malondialdehyde (MDA) and/or oxidation lag time of low-density lipoproteins (LDL) ex vivo. The Panel considers that both TBARS and MDA, when used alone, are not reliable markers of lipid peroxidation (Griffiths et al., 2002; Lykkesfeldt, 2007; Knasmuller et al., 2008). The Panel also considers that no evidence has been provided to establish that the oxidation lag time of LDL particles ex vivo predicts the resistance of LDL particles to oxidation in vivo (Griffiths et al., 2002; Lapointe et al., 2006; Verhoye and Langlois, 2009). Thus, for claims supported by references to human studies on the overall antioxidant capacity of plasma only, or on MDA/TBARS/oxidation lag time of LDL particles ex vivo as the only markers of lipid peroxidation, either alone on in combination with animal and/or in vitro studies, the Panel considers that a cause and effect relationship has not been established between the intake of the food/food component and the claimed effect. A number of in vitro studies were provided which addressed the antioxidant properties of different food(s)/food constituent(s), either by testing their capacity to scavenge free radicals under controlled conditions or by testing their capacity to prevent or delay protein, lipid or DNA oxidation in different in vitro models. Also, studies were provided on the relationship between the intake of the food(s)/food constituent(s) and the claimed effect by measuring markers of protein, lipid and/or DNA oxidation in animals, either in vivo or ex vivo. The Panel considers that the evidence provided in the animal and in vitro studies submitted is not sufficient to predict the occurrence of an effect of the food(s)/food constituent(s) on the protection of body cells and molecules from oxidative damage in vivo in humans. The Panel considers that while effects shown in animal and in vitro studies may be used as supportive evidence, human studies are required for substantiation of a claim. Thus, for claims supported by references to animal studies and/or in vitro studies only, the Panel considers that a cause and effect relationship has not been established between the consumption of the food/food component and the claimed effect. The Panel concludes that a cause and effect relationship has not been established between the consumption of the food(s)/food constituent(s) evaluated in this opinion and the protection of body cells and molecules such as DNA, proteins and lipids from oxidative damage.

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ID 3646 - Fiołek wonny

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