Natural Carotenoids

D. Skin Protection

• 1. Carotenoid supplementation reduces erythema in human skin after simulated solar radiation exposure.

  Lee, J. et al. (2000). Carotenoid supplementation reduces erythema in human skin after simulated solar radiation exposure. Proceedings of the Society Experimental Biology Medician. 223(2):170-4.

  Excessive exposure to solar radiation, especially ultraviolet A (UVA: 320-400 nm) and ultraviolet B (UVB: 290-320 nm) radiation, may induce UV-carcinogenesis and erythema in the skin. Although the protective effects of carotenoids against skin lesions are still unclear, beta-carotene has been proposed as an oral sun protectant. The purpose of this study was to determine the magnitude of the protective effects of oral alpha- and beta-carotene supplementation for 24 weeks on UVA- and UVB-induced erythema in humans. While being exposed to UVA and UVB radiation, 22 subjects (11 men and 11 women) were supplemented with natural carotenoids for 24 weeks. Each day for the first 8 weeks, subjects were given 30 mg of natural carotenoids containing 29.4 mg of beta-carotene, 0.36 mg of alpha-carotene, and traces of other carotenoids in vegetable oil. The natural carotenoid dose was progressively raised by 30-mg increments, at every 8 weeks, from 30 mg to 90 mg. Small areas (1 cm2) of the skin were exposed to increasing doses of UV light (16-42 mJ/cm2) to determine the minimal erythema dose (MED). MED was defined as a uniform pink color with well-defined borders. MED readings were obtained by visual inspection 24 hr postirradiation. Blood samples taken during supplementation were used to determine alpha- and beta-carotene serum levels and for a lipid peroxidation analysis. During natural carotenoid supplementation, the MED of solar simulator radiation increased significantly (P<0.05). After 24 weeks of supplementation, serum beta-carotene levels were increased from 0.22 microg/ml (95% CI; 0.16-0.27) to 1.72 microg/ml (95% CI;1.61-1.83). Similarly, alpha-carotene serum levels increased from 0.07 microg/ml (95% CI;0.048-0.092) to 0.36 microg/ml (95% CI; 0.32-0.40). Serum lipid peroxidation was significantly (P<0.05) inhibited in a dose-dependent manner during natural carotenoid supplementation. The present data suggest that supplementation with natural carotenoids may partially protect human skin from UVA- and UVB-induced erythema, although the magnitude of the protective effect is modest.

• 2. The antioxidant effect of palm fruit carotene on skin lipid peroxidation in guinea pigs as estimated by chemiluminescence-HPLC method

  Miyazawa, T. et al. (1994). The antioxidant effect of palm fruit carotene on skin lipid peroxidation in guinea pigs as estimated by chemiluminescence-HPLC method. Journal of Nutritional Science and Vitamology. 40(4):315-24.

  To study the antioxidant effect of palm fruit carotene on skin lipid peroxidation, the guinea pigs were orally fed ad libitum palm fruit carotene, beta-carotene, or vehicle emulsions, in which carotene (0.05%, w/w) was suspended in drinking water. After treatment of carotene for 12 weeks, animals were exposed to ultraviolet ray (UV), and squalene monohydroperoxide (SqOOH)/squalene (Sq) ratios in the skin lipid were analyzed using the chemiluminescence-HPLC method. Carotene accumulation was found in the skin of guinea pigs that were orally administered palm fruit carotene or beta-carotene. After UV irradiation, especially immediately after, the rise in the SqOOH/Sq ratio was effectively suppressed in both carotene-drinking groups in contrast with the control (carotene-untreated) group. An inverse correlation between the carotene content and the SqOOH/Sq ratio in the skin was also observed. The results suggested that palm fruit carotene intake prevents skin lipid peroxidation caused by UV irradiation.

• 3. Carotenoids and protection against solar UV radiation.

  Sies, H. et al. (2002). Carotenoids and protection against solar UV radiation. Skin pharmacology and applied skin physiology. 15(5):291-296.

  Upon exposure to UV light photooxidative reactions are initiated which are damaging to biomolecules and affect the integrity of cells and tissues. Photooxidative damage plays a role in pathological processes and is involved in the development of disorders affecting the skin. When skin is exposed to UV light, erythema is observed as an initial reaction. Carotenoids like beta-carotene or lycopene are efficient antioxidants scavenging singlet molecular oxygen and peroxyl radicals generated in during photooxidation. When beta-carotene was applied as such or in combination with alpha-tocopherol for 12 weeks, erythema formation induced with a solar light simulator was diminished from week 8 on. Similar effects were also achieved with a diet rich in lycopene. Ingestion of tomato paste corresponding to a dose of 16 mg lycopene/ day over 10 weeks led to increases in serum levels of lycopene and total carotenoids in skin. At week 10, erythema formation was significantly lower in the group that ingested the tomato paste as compared to the control group. No significant difference was found at week 4 of treatment. Thus, protection against UV light-induced erythema can be achieved by ingestion of a commonly consumed dietary source of lycopene. Such protective effects of carotenoids were also demonstrated in cell culture. The in-vitro data indicate that there is an optimal level of protection for each carotenoid.

• 4. Effect of beta-carotene supplementation on the human sunburn reaction

  Marjan et al. Experimental Dermatology. Volume 4, Issue 2, pages 104–111, April 1995

  Beta-carotene, a quencher of excited species such as singlet oxygen and free radicals, has been reported to protect against cutaneous photodamage, including sunburn acutely and photocarcinogenesis chronically. The present double blind placebo-controlled study examines the ef-tect of beta-carotene supplementation on the human sunburn response and specifically on the induction of sunburn cells at the time of peak reaction intensity (24 h) after a single solar simulated light exposure 3 times the individually determined minimal erythema dose (MED). Administered orally either as a single 120 mg dose to dietarily restricted subjects or for 23 d as a daily 90 mg supplement to subjects on standard diets, beta-carotene increased plasma and skin levels of beta-carotene compared to both pretreatment levels and placebo-treated controls, but provided no clinically or histologically detectable protection against a 3 MED sunburn reaction. Thus, these data suggest that oral beta-carotene supplementation is unlikely to modify the severity of cutaneous photodamage in normal individuals to a clinically meaningful degree.

• 5. Topical beta-carotene is converted to retinyl esters in human skin ex vivo and mouse skin in vivo

  Antille et al. Exp Dermatol. 2004 Sep;13(9):558-61.

  Human epidermis contains endogenous retinoids (retinol and retinyl esters) and carotenoids (mostly beta-carotene). Previous studies have shown that the enzymes involved in retinoid metabolism are present in human epidermis. There is still a controversy about the presence in the skin of the enzymes able to convert beta-carotene into vitamin A (retinol), although a recent study demonstrated the conversion of beta-carotene into retinol in human cultured epidermal cells. In this study, we addressed the question of the possible bioconversion of topical beta-carotene into vitamin A or derivatives by human and mouse skin. Surgically excised human abdominal skin was mounted on Franz perfusion chambers to assess the cutaneous penetration of topical beta-carotene as well as its metabolism, after a 24-h incubation period, whereas hairless mice received topical beta-carotene 24 h before assaying epidermal beta-carotene and retinoid concentrations. Epidermal retinoid and beta-carotene concentrations were determined by high-pressure liquid chromatography. Topical beta-carotene penetrated well into human and mouse epidermis and induced a 10-fold (human) and a threefold (mouse) increase of epidermal retinyl esters, which demonstrates that topical beta-carotene is converted into retinyl esters by human and mouse epidermis and thus appears as a precursor of epidermal vitamin A.