ID 1510 - Koenzym Q10

PL: Koenzym Q10
EN: Co-Enzyme Q 10
Pdf: coenzyme Q10

Oświadczenie (2)

1. Charakterystyka żywności / składnika

The food constituent that is the subject of the health claim is coenzyme Q10 (ubiquinone).
Coenzyme Q10 (CoQ10) is part of the ubiquinone family of compounds, all containing 1,4 benzoquinone as the functional group with a side chain of isoprenyl units, which is 10 units in the case of coenzyme Q10. Coenzyme Q10 can exist in three oxidation states: the fully reduced ubiquinol form (CoQ10H2), the radical semiquinone intermediate (CoQ10H) and the fully oxidised ubiquinone form (CoQ10). Coenzyme Q10 can be synthesised in most human tissues and occurs widely in nature, including foods, mainly in meat, poultry and fish. Coenzyme Q10 is measurable in foods by established methods.
The Panel considers that the food constituent, coenzyme Q10 (ubiquinone), which is the subject of the health claims, is sufficiently characterised.

2.3. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1510)

The claimed effects are “antioxidant activity” and “normal antioxidant properties”. 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 relate to the protection of 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 biologically relevant 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. Naukowe uzasadnienia wpływu na zdrowie człowieka

Coenzyme Q10 (ubiquinone) is found in high concentrations in the mitochondria, it is involved in the mitochondrial electron transport chain as an electron acceptor/donor, and is known to play a role in oxidative mitochondrial phosphorylation (ATP production). Coenzyme Q10 can be synthesised by the body and there is no need for coenzyme Q10 in human diets (SCF, 1993).

3.3. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1510)

Most of the references provided were narrative reviews on the (biochemical) functions of coenzyme Q10 and its potential role in disease prevention and treatment, especially cardiovascular disease. The Panel considers that no conclusions can be drawn from these references for the scientific substantiation of the claimed effect. Also, a number of human studies on the effects of coenzyme Q10 supplementation on the antioxidant capacity of plasma (e.g. assessed by the TRAP method) were cited. The Panel notes that this measure is a marker of antioxidant status and does not assess oxidative damage to molecules.
Six human intervention studies on effects of coenzyme Q10 supplementation on lipid peroxidation were cited (Alleva, 1995; Stocker et al., 1991, revised by Kaikkonen et al., 2002; Mohr et al., 1992; Singh et al., 2005; Weber et al., 1994; Kontush et al., 1994).
Three human intervention studies were presented on the effects of coenzyme Q10 supplementation (from 30 to 100 mg/day) on LDL resistance to oxidation ex vivo (lag time) assessed by different methods (Alleva, 1995; Stocker et al., 1991, revised by Kaikkonen et al., 2002; Mohr et al., 1992). Also, a cross-sectional study on the association between the rate of (induced) oxidative modification of LDL and its ubiquinol-10 content in healthy blood donors (Kontush et al., 1994) was provided. The Panel notes that LDL resistance to oxidation ex vivo is not a reliable marker of lipid peroxidation (Griffiths et al., 2002).
Three human intervention studies were presented on the effects of coenzyme Q10 supplementation (from 90 to 200 mg/day) on plasma concentrations of malondialdehyde (MDA) and/or thiobarbituric acid reactive substances (TBARS) and/or lipid hydroperoxides (Stocker et al., 1991, revised by Kaikkonen et al., 2002; Singh et al., 2005; Weber et al., 1994). The Panel notes that measuring TBARS is not an accepted method to assess lipid peroxidation (non specific) and that MDA and lipid hydroperoxides measured by HPLC are not reliable markers of lipid peroxidation when used alone (Griffiths et al., 2002; Lykkesfeldt, 2007; Knasmüller et al., 2008).
Two rat studies on the effect of supplementation with coenzyme Q10 on DNA strand breaks were presented (Quiles et al., 2004; 2005), as well as one in vitro study with human lymphocytes (Tomasetti et al., 1999). The Panel considers that the evidence provided in animal and in vitro studies does not predict an effect of coenzyme Q10 consumption on the protection of DNA from oxidative damage in humans, and that no scientific conclusions can be drawn from these studies for the substantiation of the claimed effect.
In weighing the evidence, the Panel took into account that LDL resistance to oxidation ex vivo is not a reliable marker of lipid peroxidation, that measuring TBARS is not an accepted method to assess lipid peroxidation, that MDA and lipid hydroperoxides measured by HPLC are not reliable markers of lipid peroxidation when used alone, and that evidence provided in animal and in vitro studies does not predict an effect on the protection of DNA from oxidative damage in humans.
The Panel concludes that a cause and effect relationship has not been established between the intake of coenzyme Q10 (ubiquinone) and protection of DNA, proteins or lipids from oxidative damage.

Warunki i możliwe ograniczenia stosowania oświadczenia

30-200 mg per day