86 SKIN CARE A B C
Figure 3: UV-B-irradiated 3D full skin models with H&E staining after 24 hours. Notes: A - Untreated control tissue, not irradiated (reference); B - Untreated tissue irradiated with 200mJ/cm2
arrows: sunburned cells, red arrows: hydropic cells or tissue, dashed white line: epidermal-dermal transition zone. Photosensitisers are endogenous or
exogenous compounds that are readily activated by UV or visible light; once activated, they cause an adverse skin reaction. This can result in the creation of ROS. Light-induced ROS and free radicals lead to oxidative stress. They wreak havoc on proteins, lipids and DNA, causing negative changes in the skin structure. Singlet oxygen is an extraordinarily reactive
molecule, and its impact on cellular DNA is particularly disastrous for the skin. When it attacks cell membranes, it activates enzymes that the lead to cell death, peroxidation and ultimately deterioration of the skin’s appearance. A singlet oxygen molecule can implant a single 8-hydroxydesoxyguanosine (8-OH-dG), a biomarker for oxidative stress into a DNA molecule. This process triggers the so-called NFkB
cascade – the beginning of inflammation, which results in a chain reaction of thousands of molecular modifications in the cell, membrane and the overexpression of MMP-1 enzymes, destroying collagen and other elastic fibres. Thus, skin ageing is accelerated.1,5
Light-induced oxidative stress & triggering factors Light-induced oxidative stress is triggered by various types of radiation, such as UV-A and UV-B radiation and infrared light. Together, these are responsible for approximately 50-80% of visual skin ageing. Therefore, light protection is an essential feature of cosmetic
formulations against premature skin ageing. In particular, the amount of UV-B in
sunlight is a critical, well-characterised factor in skin damage. UV-B radiation, a high-energy, short-wavelength radiation (290-320 nm), basically stresses the epidermal part of the skin. In extreme cases, this leads to severe sunburns and damage to the apical, as well as proliferating basal keratinocytes.6 In contrast, the UV-A portion of sunlight is
lower in energy and longer in wavelength (320- 400 nm). This type of irradiation can penetrate the dermal parts of the skin, resulting in long- term damage to collagen and elastin fibres. Long-term and combined irradiation of human skin with UV-B and UV-A leads to reduction and deceleration of the skins renewal potential, as well as structural damage to the dermal matrix, which eventually results in permanent physical relaxation of the skin. Human skin possesses intrinsic cellular
protective mechanisms capable of regulating the externally-induced amount of ROS to a tolerable minimum. This natural protective mechanism can be overloaded by regular and continuous UV irradiation, weakening more and more over time. Sunscreen filters, such as zinc oxide and
titanium oxide, can ward off some of the radiation affecting our skin, but not all of it. Complementary ingredients like antioxidants play a key role in cosmetic formulations to prevent premature photo-ageing of the skin and act as a supplement to sunscreen filters.7
Astaxanthin: Proven cell protection The positive properties of astaxanthin for protection against the effects of UV radiation have been confirmed with the active ingredient AstaCos OL50 in both in vivo and in vitro studies. In one in vitro study, keratinocytes exposed to intense UV-B radiation were compared: prior to irradiation, keratinocytes were treated with a concentration of 0.05% AstaCos OL50. Compared to the untreated, non-irradiated
reference tissue (Figure 3b), severe tissue damage of all epidermal layers was detected. The untreated, irradiated models showed clear signs of excessive UV irradiation and sunburned cells (yellow arrows) – indicated by constricted nuclei. Hydropic cells and areas (red arrows) with less intense staining could be identified, having caused cytosolic fluid accumulation. In addition, numerous vacuolated
keratinocytes were found in the epidermis, reflecting typical tissue destruction after strong exposure to UV light as well as incipient parakeratosis. Compared to the untreated irradiated skin models, the tissue treated with 0.05% AstaCos OL50 showed a much milder UV-B phenotype without parakeratosis (Figure 3c). The tissue was less vacuolated, and contained fewer apoptotic cells and vacuolated keratinocytes. Moreover, significantly fewer sunburned cells (yellow arrows) and apoptotic cells were found compared to the positive control. Overall, epidermis treated with the product
left a healthier, more vital impression, and surviving basal keratinocytes still exhibited the typical elongated morphology (Figure 3a). This indicates that basal keratinocytes are largely unaffected by UV irradiation. The results of the described in vitro study confirm the declaration that AstaCos OL50 has a strong protective effect against UV-B radiation in the reconstructed 3D human skin models. The protective effect against the impacts
of UV radiation of AstaCos OL50 was also confirmed in an in vivo pilot clinical study performed at the Medical University of Graz, using a vehicle emulsion with 0.2% AstaCos OL50 (Figure 4). In a controlled experimental setting, its UV-protective effect compared to placebo was tested on 21 healthy volunteers with Fitzpatrick skin type 2 or 3. After intensive exposure to UV light, a 25%
Figure 4: Measurement with Skintrek PT3 exposure unit of erythema formation PERSONAL CARE October 2021
lower erythema level was measured with the AstaCos OL50 treatment compared to the placebo group (Figure 5). In this experimental setting, the active ingredient suppressed visible erythema formation in over 70% of the cases.8
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(positive control); C - 0.05% tissue treated with AstaCos OL 50 after irradiation with 200mJ/cm2
. Yellow
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