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.

2.3. Redukcja zmęczenia mięśni podczas ćwiczeń (ID 1840)

The claimed effect is “physical performance and condition”. The Panel assumes that the target population is active individuals in the general population.
In the context of the proposed wordings, the Panel assumes that the claimed effect refers to the reduction of muscle fatigue during exercise.
The Panel considers that reduction of muscle fatigue during exercise is a beneficial physiological effect.

2.4. Wpływ na układ odpornościowy (ID 2304, 3160)

The claimed effect is “endogenous antioxidant enzyme; effects on immune system”. The Panel assumes that the target population is the general population.
The claimed effect “effects on immune system” is not sufficiently defined and no further details were provided in the proposed wording. The scientific references submitted report on either animal or ex vivo studies with human cells on outcomes which did not help to clarify the claimed effect. One human study in HIV positive subjects is presented in poster form without sufficient details for its evaluation.
The Panel considers that the claimed effect is general and non-specific and does not refer to any specific health claim as required by Regulation (EC) No 1924/2006.

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.

3.3. Redukcja zmęczenia mięśni podczas ćwiczeń (ID 1840)

Eight references were provided for the scientific substantiation of this claim. Most of the references reported on foods (flower pollen extracts with unknown SOD content) other than SOD, and/or on outcomes other than the claimed effect (e.g. upper respiratory infections, chronic prostatitis, benign prostate hyperplasia, etc.). The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect.
One of the references provided reported on a study that investigated the effects of a pollen extract exhibiting SOD-activity on muscle-related outcomes during exercise before and after an intervention period (Krotkiewski et al., 1994). A total of 50 subjects were “allocated” to consume a pollen pistil extract (SOD activity reported to be 30,000 IU/g, total daily dose not reported, n=36) or placebo (n=14) for four weeks. At the beginning and end of the study, all subjects completed an alternate stepping plus cycling exercise of approximately 140 minutes duration. Heart rate was monitored at the different work loads during the bicycling and peak isokinetic and isometric strength were tested in a Kin-Com dynamometer. Lactate concentrations in plasma and muscle were assessed before and after each exercise bout. Muscle pain, oedema, tenderness and discomfort were self-rated by the subjects using a visual analogue scale in five consecutive days after the exercise bouts. Heart rate at the different work loads during the bicycling was reported to be uninfluenced by the intervention or placebo. No difference in peak isokinetic and isometric strength was detected in either of the groups. No direct measurements of muscle fatigue, endurance capacity or performance were performed during exercise. The Panel notes that the dose of SOD used in this study is not reported, that no direct measurements of muscle fatigue, endurance capacity or performance were performed during exercise, and that no information regarding the validity of the visual analogue scales used to assess muscle pain, oedema, tenderness and discomfort was provided. The Panel considers that no conclusions can be drawn from this reference 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 reduction of muscle fatigue during exercise.