ID 2305 -
Dysmutaza ponadtlenkowa
PL: Dysmutaza ponadtlenkowa
EN: Superoxide dismutase (SOD)
Pdf: superoxide dismutase
Oświadczenie (2)
- antyoksydacyjne
- endogennych enzymów antyoksydacyjnych, wpływ na układ odpornościowy
- endogennych enzymów antyoksydacyjnych, chroni skórę przed słońce szkoda
- endogennych enzymów antyoksydacyjnych, ogólne korzyści suplementacji antyoksydacyjne SOD
- stan psychiczny i wydajność antioxidativity
- właściwości antyoksydacyjne
1. Charakterystyka żywności / składnika
The food constituents that are the subjects of the health claims are “superoxide dismutase (SOD)”, “melon extract (containing SOD)/wheat gliadin”, and “pollen pistil extract + SOD”.
Superoxide dismutases (SOD) comprise a class of enzymes that convert the superoxide anion radical into hydrogen peroxide and oxygen. The type of SOD that is the subject of the claim is not specified (amino acid sequence and mineral cofactor). However, enzymatic activity of SOD can be measured by established methods and can be used to standardise its content in foods. Gliadin is a glycoprotein present in wheat and other cereals. Gliadin is used to protect enzymes (e.g. SOD) against stomach acid-induced breakdown.
The Panel assumes that the food constituent that is the subject of the health claims (i.e. the “active” food constituent responsible for the claimed effect) is SOD. The Panel notes that absorption of intact SOD has not been observed in humans and is unlikely to occur.
The Panel considers that the food constituent, superoxide dismutase, which is the subject of the health claims, is sufficiently characterised in relation to the claimed effects.
2.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1785, 1839, 1970, 2304, 2305, 3159, 3160)
The claimed effects are “antioxidant activity”, “mental state and performance/antioxidativity”, “antioxidant properties”, “endogenous antioxidant enzyme; effects on immune system”, “endogenous antioxidant enzyme; general antioxidant benefits of SOD supplementation” and “endogenous antioxidant enzyme, protects skin from sun damage”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effects refer to the protection of body cells and molecules from oxidative damage caused by free radicals.
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 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.
2.2. Ochrona skóry przed uszkodzeniem promieniami ultrafioletowymi (UV) (ID 2305, 3161)
The claimed effect is “endogenous antioxidant enzyme, protects skin from sun damage”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to UV- dependent premature aging of the skin related to photo-oxidative damage of skin structure and texture.
Skin aging and premature skin aging is related to UV-induced photo-oxidative reactions which activate matrix-metallo-proteinases that degrade extracellular matrix proteins including collagen.
The Panel considers that protection of the skin from photo-oxidative (UV-induced) damage is a beneficial physiological effect.
3.1. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1785, 1839, 1970, 2304, 2305, 3159, 3160)
Six of the references provided investigated the effects of SOD on measures of antioxidant status and/or oxidative stress in humans. Five of the studies used Glisodin®, a food supplement containing cantaloupe melon extract with SOD and gliadin (a wheat protein).
Arent et al. (2004) tested the effects of a blend containing a mixture of SOD, CoQ10 and beta-glucans on oxidative stress in 22 male soccer players. The Panel considers that no conclusions can be drawn from this study with respect to the role of SOD alone on the claimed effect.
Hong et al. (2004) described in a meeting report an open label, uncontrolled intervention study in which Glisodin® (1500 IU SOD per day) was administered to 44 healthy volunteers for a period of four weeks. The Panel considers that no conclusions can be drawn from this uncontrolled study for the scientific substantiation of the claim.
Muth et al. (2004) reported on a double blind randomised placebo-controlled study which investigated the effects of Glisodin® (1000 IU SOD per day) on hyperbaric oxygen (HBO)-induced oxidative stress in male trained scuba divers (n=10) vs. placebo (wheat gliadin alone, n=10). After two weeks of intervention, subjects were exposed to 100 % oxygen breathing (two periods of 30 minutes each with 10 minutes of normal breathing in between). Concentrations of reduced and oxidised glutathione (GSH and GSSG, respectively), and SOD, glutathione peroxidase (GPx) and catalase activities were measured in whole blood. The alkaline comet assay was used to assess the mean tail moment in cells. Red cell malondialdehyde (MDA) content was measured using the reaction of MDA with diethyl- thiobarbituric acid. Plasma 8-isoprostane concentrations were measured using an immunoassay kit for which cross-reactivity with other metabolites of arachidonic acid is not reported. The Panel notes the small number of subjects recruited and considers that none of these measurements constitutes a reliable marker of oxidative damage to cells or molecules (see also EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA), 2010).
A research letter by Chenal et al. (2006) described a randomised double-blind placebo controlled intervention on the effects of a melon extract containing SOD (1000 IU per day) with (Glisodin ®, n=11) or without gliadin (n=12) in HIV-1 infected African subjects for three weeks. Placebo (n=12) and healthy controls (n=30) were included. Antioxidant status (not further defined in the paper) and SOD, GPx and catalase activities were assessed in plasma. Cloarec et al. (2007) reported on a randomised, placebo controlled intervention which assessed the effects of Glisodin® administration (2 x 250 IU SOD per day) for two years on MDA (MDA kit, spectrofluorometry) and on SOD and GPx activities. Introna et al. (1997) described the effect of a single dose of 10 g of Dismuzyme (1500 µg SOD) on erythrocyte-SOD (Cu-Zn SOD) activity in six volunteers vs. four controls. The Panel notes that none of the measurements performed in these studies constitutes a reliable marker of oxidative damage to cells or molecules (see also EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA), 2010).
The Panel considers that no conclusions can be drawn from any of the studies presented for the scientific substantiation of the claimed effect.
The Panel concludes that a cause and effect relationship has not been established between the consumption of SOD and the protection of DNA, proteins and lipids from oxidative damage.
3.2. Ochrona skóry przed uszkodzeniem promieniami ultrafioletowymi (UV) (ID 2305, 3161)
A total of 27 references were provided for the scientific substantiation of this claim.
None of the references provided assessed the effects of SOD consumption in preventing photo- oxidative damage to the skin whereas four references assessed the protection of skin from sun damage.
Laverdet (2003) and Laverdet et al. (2005) reported on an open label, uncontrolled intervention study where Glisodin® (2 x 250 mg per day) was administered for two months to 15 adult patients (11 females) suffering from fragile skin or hypersensitivity to sun. The Panel considers that no conclusions can be drawn from this uncontrolled study for the scientific substantiation of the claimed effect.
The other two papers (Mac-Mary et al., 2005; 2007) described the same randomised, double-blind, placebo-controlled study in which 50 healthy volunteers of phototype II, III and IV were randomised to consume Glisodin® (2 x 250 mg per day) or placebo for a period of four weeks. No statistically significant differences between the intervention and placebo groups were found with respect to changes in the Minimum Erythematal Dose (MED) or in the erythemal response (reddening and vascularisation).
The Panel concludes that a cause and effect relationship has not been established between the consumption of SOD and protection of the skin from photo-oxidative (UV-induced) damage.
Warunki i możliwe ograniczenia stosowania oświadczenia
500 mg equivalent to 500 IU (NBT units) for 1 to 2 months