ID 2081 -
Likopen
PL: Likopen
EN: Lycopene
Pdf: lycopene
Oświadczenie (2)
- właściwości antyoksydacyjne / ochrona dna
- prostaty zdrowia
- utrzymuje układ sercowo-naczyniowy
- dla systemu antyoksydacyjnego / ochrony DNA
- właściwości antyoksydacyjne
- Kontrola stresu oksydacyjnego
- utrzymuje zdrowia prostaty
- właściwości antyoksydacyjne / komórki i ochrony dna
1. Charakterystyka żywności / składnika
The food constituent that is the subject of the health claims is lycopene (psi, psi-carotene).
Lycopene is a well recognised dietary constituent and is measurable in foods, blood and tissues by established methods. Major dietary sources of lycopene are tomatoes and tomato products. Lycopene is also the natural red colorant of water melons, pink grapefruit and rose hips. Dietary sources of lycopene, or lycopene preparations from natural sources, usually contain other food constituents (e.g. other carotenoids and/or polyphenols) which may contribute to the claimed effects. Synthetic lycopene has recently been authorised in the EU as a novel food ingredient6. The present opinion applies to lycopene from all sources with appropriate bioavailability in the specified amounts.
The Panel considers that the food constituent, lycopene, which is the subject of the health claims, is sufficiently characterised.
2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1608, 1609, 1611, 1662, 1663, 1664, 1899, 1942, 2081, 2082, 2142, 2374)
The claimed effects are “antioxidant properties”, “antioxidant properties/cell and DNA protection”, “antioxidant properties/protection of DNA”, “oxidative stress control”, “for antioxidant protection system/protection of DNA”, “maintains cardiovascular health”, “prostate health” and “maintains prostate health”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings and clarifications provided by Member States, the Panel assumes that the claimed effects refer to the protection of DNA, proteins and lipids from oxidative damage.
The Panel considers that claims made on the antioxidant capacity/content of lycopene-containing foods based on their capability to scavenge free radicals in vitro refer to a property of the food/food
constituent measured in model systems, and that the information provided does not establish that this exerts a beneficial physiological effect in humans as required by Regulation (EC) No 1924/2006.
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 and pollutants). These reactive intermediates damage molecules such as DNA, proteins and lipids if they are not intercepted by the antioxidant network, which includes free radical scavengers such as antioxidant nutrients.
The Panel considers that protection of DNA, proteins and lipids from oxidative damage may be a beneficial physiological effect.
3.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1608, 1609, 1611, 1662, 1663, 1664, 1899, 1942, 2081, 2082, 2142, 2374)
A number of the references provided were narrative reviews or consensus opinions on the health effects of lycopene that did not allow evaluation of original data, reports on intervention studies that assessed the effects of other carotenoids or antioxidant vitamins, either alone or in combination with
lycopene, or human studies assessing the effects of lycopene intake and related products on health outcomes unrelated to the claimed effect (e.g. UV-induced erythema, UV-induced immunomodulation and the risk of chronic disease, such as prostate cancer). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
Some experimental, and generally small-scale, human studies investigated the effects of lycopene consumption on the total antioxidant activity of plasma measured by various assays (i.e. trolox-equivalent antioxidant capacity (TEAC), total reactive antioxidant potential (TRAP), and a chemiluminescent assay using 2, 2'-azinobis (3-ethylbenzothiazoline-6-sulfonate) (ABTS) as a reagent (Bohm and Bitsch, 1999; Neyestani et al., 2007; Tyssandier et al., 2004)); on GSH concentrations and antioxidant metalloenzyme activities (Hininger et al., 2001); on DNA strand breaks (Briviba et al., 2004a; Pool-Zobel et al., 1997; Porrini et al., 2005; Zhao et al., 2006); on ex vivo DNA oxidation (e.g. to lymphocytes) measured by different modifications of the comet assay (e.g. after challenge with Fe2+ or with hydrogen peroxide before electrophoresis (Riso et al., 1999; 2004; Torbergsen and Collins, 2000; Zhao et al., 2006)); on ex vivo susceptibility of LDL to Cu-ion induced oxidation (Briviba et al., 2004b; Carroll et al., 2000; Fuhrman et al., 2000; Hininger et al., 2001; Maruyama et al., 2001; Silaste et al., 2007; Visioli et al., 2003); on LDL conjugated dienes (Agarwal and Rao, 1998), on the formation of malondialdehyde (MDA) measured as thio-barbituric acid reactive substances (TBARS) (Agarwal and Rao, 1998; Briviba et al., 2004b; Neyestani et al., 2007; Rao and Agarwal, 1998; Rao and Shen, 2002); and on protein thiol concentrations (Hininger et al., 2001; Rao and Agarwal, 1998). The Panel notes that measurements of the total antioxidant activity/potential of plasma, and/or of GSH concentrations, and/or of antioxidant enzyme activities are not considered to be markers of oxidative damage, that the formation of MDA measured as TBARS, as well as the resistance of LDL to oxidation, are not suitable markers to assess lipid peroxidation, that the variants of the comet assay which measure unspecified DNA damage do not reflect DNA oxidative damage but general DNA strand breaks independent of their origin, that the ex vivo DNA resistance to oxidation after oxidative challenge does not reflect in vivo DNA oxidative damage, and that measurement of protein thiol concentrations is not a reliable marker of oxidative damage to proteins (Dalle-Donne et al., 2006; Dragsted, 2008; Griffiths et al., 2002; Knasmuller et al., 2008; Mayne, 2003). In addition, a number of the human studies provided were uncontrolled interventions with lycopene or tomato products (Agarwal and Rao, 1998; Bohm and Bitsch, 1999; Bowen et al., 2002; Hadley et al., 2003; Pool-Zobel et al., 1997; Porrini and Riso, 2000; Rao and Shen, 2002; Riso et al., 2004; Tyssandier et al., 2004; Visioli et al., 2003). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
Rao and Agarwal (1998) performed a controlled, randomised, cross-over study with five different sources of lycopene in 19 healthy subjects (9 females/10 males), who were non-smokers aged 25- 40 years. The duration of the study was one week with each source providing lycopene at 20.5 mg/day (spaghetti sauce A), 39.2 mg/day (spaghetti sauce B), 50.4 mg/day (tomato juice), 75 mg/day (tomato oleoresin A) and 150 mg/day (tomato oleoresin B). Controls received a placebo which was not further specified. As a marker of DNA damage, 8-oxodG in lymphocytes was measured by HPLC with EC detection. For lipid peroxidation, TBARS were determined in serum, and protein oxidation was estimated by loss of free thiol groups in serum measured with beta dystrobrevin (5,5'-Dithio-bis (2- nitrobenzoic acid), DTNB). There was no statistically significant difference in DNA oxidation between the different verum groups and placebo. The Panel notes that TBARS and loss of free thiol groups in serum measured with DTNB are not reliable markers of oxidative damage to protein and lipids, respectively.
Kucuk et al. (2002) performed a randomised, two-arm clinical intervention study in patients with prostate cancer scheduled for radical prostatectomy. Data were collected from 26 patients and the intervention group took 30 mg of lycopene as tomato oleoresin for three weeks. Levels of 5-OHmdU (5-hydroxy-methyl-desoxy-uridine) in peripheral blood lymphocytes were not significantly different between groups before and after intervention.
In weighing the evidence, the Panel took into account that none of the studies provided reported a significant effect of lycopene consumption on reliable markers of oxidative damage to DNA, lipids or proteins compared to control.
The Panel concludes that a cause and effect relationship has not been established between the consumption of lycopene and protection of DNA, proteins and lipids from oxidative damage.
Warunki i możliwe ograniczenia stosowania oświadczenia
7-16 mg/day