2.1. Poprawa rozszerzenia naczyń krwionośnych zależnego od śródbłonka (ID 1649, 1783)

The claimed effects are “vascular health” and “circulatory system”. The Panel assumes that the target population is the general population.
In the context of the proposed wordings and the clarifications provided by Member States, the Panel assumes that the claimed effect refers to the improvement of endothelial function.
Endothelial function is not sufficiently defined for a scientific evaluation, owing to the fact that endothelium-derived active factors play a role in the maintenance of several functions of the vascular system, including vasomotion, smooth muscle proliferation, thrombosis, inflammation, coagulation, fibrinolysis, and oxidation that can be studied by indirect methods. However, from the clarifications provided by Member States, the Panel assumes that the claimed effect refers to the role of
endothelium in increasing arterial compliance in response to an increased blood flow (i.e. endothelium-dependent vasodilation).
The Panel considers that improvement of endothelium-dependent vasodilation may be a beneficial physiological effect.

2.2. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1784)

The claimed effect is “antioxidant properties”. The Panel assumes that the target population is the general population.
In the context of the proposed wording, the Panel assumes that the claimed effect refers to the protection of cells and molecules from oxidative damage.
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.

3.1. Poprawa rozszerzenia naczyń krwionośnych zależnego od śródbłonka (ID 1649, 1783)

Four references were provided for the scientific substantiation of this claim. These are an information sheet about rutin (posted on the internet in a company web site) which does not include original data, a drug manual, a narrative review of the health effects of flavonoids in general and an ex vivo study on the effects of rutin on the relaxation of arterial smooth muscle cells from rats (Fusi et al., 2003). The Panel considers that no conclusions can be drawn from these references 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 rutin and the improvement of endothelium-dependent vasodilation.

3.2. Ochrona DNA, białek i lipidów przed uszkodzeniem oksydacyjnym (ID 1784)

Two references were provided for the scientific substantiation of this claim. One was an information sheet about rutin (posted on the internet in a company web site) which does not include original data. The second reference reported on a randomised, single-blind placebo controlled trial in which 18 healthy female volunteers (18-48 years) consumed a supplement containing 500 mg per day of rutin or an equivalent dose of glucose monohydrate (placebo) for six weeks (Boyle et al., 2000). At the beginning and at the end of the study the following indicators/markers were measured: plasma flavonoid, ascorbic acid, tocopherol and carotenoid concentrations using high-performance liquid chromatography (HPLC); plasma antioxidant capacity using the ferric reducing ability of plasma (FRAP) assay; the malondialdehyde (MDA) content of urine and plasma determined by resolution of the TBA-MDA adduct using isocratic reverse-phase HPLC with fluorimetric detection; oxidised glutathione (GSSG) quantified by measuring the total glutathione present after the derivatisation of reduced glutathione (GSH) with 2-vinyl pyridine; lymphocyte DNA damage by using the comet assay, which measures strand breaks and oxidised pyrimidines; urinary 8-hydroxy-2-deoxyguanosine
concentrations using a competitive ELISA assay; and urinary 8-iso-prostaglandin F2 using a commercial ELISA kit.
The Panel notes that plasma concentrations of flavonoids, ascorbic acid, tocopherols and carotenoids, and measures of the antioxidant capacity of plasma, may be indicators of antioxidant status but are not considered as markers of oxidative stress, and that lymphocyte DNA damage assessed by using the comet assay which measures strand breaks and oxidised pyrimidines is not an accepted method to
assess oxidative damage of DNA. The Panel also notes that urinary 8-iso-prostaglandin F2 is a well accepted marker of lipid peroxidation, and that MDA assessed by HPLC, urinary 8-hydroxy-2-deoxyguanosine concentrations using a competitive ELISA assay, and GSSG quantified by measuring the total glutathione present after the derivatisation of GSH with 2-vinyl pyridine could be used as supportive markers of oxidative damage. No significant differences between the intervention and placebo groups were observed in relation to changes in urinary 8-iso-prostaglandin
F2 , MDA or GSSG/GSH during the study.
The Panel notes that the only human intervention study provided does not support an effect of rutin consumption on the protection of DNA, proteins or lipids from oxidative damage.
The Panel concludes that a cause and effect relationship has not been established between the consumption of rutin and the protection of DNA, proteins and lipids from oxidative damage.