Oxidative stress reflects an imbalance between the systemic manifestation of ROS and a biological system’s ability to readily detoxify the reactive intermediates or to repair the resulting damage. Radiation, smoking and bad diet can influence oxidative stress. Multiple studies show the relationship between these factors and carotenoid concentrations, values of antioxidant or oxidative status [1] [2]. But there may of course be other factors creating and mediating oxidative stress such as illness, psychological stress or fatigue.
When analyzed by a chemical assay based on urinary malondialdehyde excretion, an indicator of oxidative lipid damage, people with high oxidative stress had significantly lower skin carotenoid levels than people with low oxidative stress. [3, 4] These observations provide evidence that skin carotenoid readings might be useful as a surrogate marker for general antioxidant status. [5]
A study done by Haag et al. [6] used electron paramagnetic resonance (EPR) spectroscopy to assess reduction of nitroxides as an indicator of antioxidant capacity of human skin and found that skin carotenoid status as assessed by RRS was correlated with the rate constant of nitroxide decrease. These observations suggest that skin carotenoid RRS scores might be useful as a surrogate marker for general antioxidant status.
General stress factors (such as fatigue, illness) have been suggested to influence skin carotenoid status but have not been quantitatively or systematically assessed in multivariate models controlling for other factors [3].
Sunlight and UV/VIS Radiation
Human skin is susceptible to free radical and ROS formation due to irradiation in the UV, visible and IR wavelength range [7]. With regard to the total sun wavelength spectrum, up to 50% of the radicals are not produced by wavelengths in the UV range [8].
Photoprotection of biological systems can be achieved by topical protection like protective clothing and sunscreens, endogenous pigments like melanin that scatter and absorb UV light or antioxidants.
According to Lademann et al. [9] sunscreens provide a topical double-track protection system against skin damage as they contain antioxidants in addition to UV filter substances.
Endogenous photoprotection mechanisms work by increasing the barrier for UV light (e.g. UV – absorbing compounds), protecting target molecules while acting as scavengers (e.g. antioxidants), repairing UV-induced damage by induction of repair systems or suppressing cellular responses (e.g. anti-inflammatory agents).
Antioxidants like carotenoids, tocopherols, flavonoids and other polyphenols as well as vitamin C are able to protect the skin not only in the UV but also in the visible and infrared spectral ranges [10]. The SPF (sun protection factor) of antioxidants is small (i.e. approximately equal to 2 [3]) and insufficient to provide protection against direct sunlight. It is enough though to reduce the unfavorable effects of indirect sunlight radiation. [11] Sies et al [12] state that while protection through individual dietary components in terms of SPF may be considerably lower than that achieved using topical sunscreens, an increased lifelong overall protection via dietary supply may contribute significantly to skin health. It is noted that most of the erythemal annual UV dose is encountered under non-vacation conditions when no sunscreen is applied. While endogenous protection in terms of SPF may be low, the cumulative effect receives increasing attention. Lifelong inadvertent sunlight exposure is important.
Dietary protection is provided by carotenoids, tocopherols, ascorbate, flavonoids or n-3 fatty acids, contributing to maintenance and resistance as part of lifelong protection [12]. According to Offord et al. [13] vitamin C, E and carnosic acid have the potential to be effective photoprotectors. The carotenoids β-carotene or lycopene must be delivered together with vitamin E to prevent formation of oxidative derivatives which may influence the cellular and molecular responses. Wrona et al. [14] showed that a combination of zeaxanthin and α-tocopherol offers synergistic protection against photosensitized lipid peroxidation in liposomal systems. Sies et al [12] note that substances may act synergistically. Vitamin C for instance regenerates tocopherol, together they increase the sunburn threshold significantly. The single compounds provided moderate but statistically not significant protection.
Mixtures of carotenoids (β-carotene, lutein and lycopene) ameliorate UV-induced erythema in humans whereas one-component supplementation of β-carotene proved less effective.
As noted in all studies so far carried out, there is a time of approximately 8 to 10 weeks until protection against erythema formation becomes significant [12].By using EPR and RRS, Meinke et al. [15] showed that a decrease in the carotenoid concentration in vivo induced by UV irradiation is explainable by the formation of radicals in the skin. Ermakov et al. [16] show a decrease of skin carotenoid levels with increased sun exposure:
IR Radiation
Darvin et al. [18] and Akhalaya [19] show that utilization of the IR irradiation in medicine can have side effects. The carotenoids β-carotene and lycopene were decreased subsequent to IR irradiation of the skin.
Schröder et al. [20, 17] state that solar radiation damages human skin by causing premature skin aging. Not only does this result from UV radiation but also from longer wavelengths, in particular near IR irradiation (IRA). IRA radiation has been demonstrated to alter the collagen equilibrium of the dermal extracellular matrix. Currently there are no specific chemical or physical filters available against IRA and existing compounds have not been shown to possess IRA -filtering capacity. Filters reflecting IRA (e.g. Titanium dioxide) might raise cosmetic issues. An alternative approach is the use of antioxidants, especially mitochondrial targeted antioxidants.
It has also been shown that topical application of β-carotene on skin can effectively neutralize free radicals which are produced on the skin surface due to IR irradiation [21]. Furthermore it was discovered that the topically applied antioxidant protects the natural antioxidant network of the skin.
Diet & Dietary Intervention
Concerning carotenoid supplementation trials, it is well known and accepted that carotenoid supplementation leads to measurable increases in carotenoids in human skin [22, 23, 24]. This obviously underlies much of the work done in the setting of using dietary sources of carotenoids for sun protection [25, 26, 27]. This also underlies the licensing of the RRS method to the nutritional supplement industry (“Biophotonic Scanner”, NuSkin/Pharmanex Inc., Provo, Utah), based on the finding that carotenoid-containing vitamin supplements produced an increase in skin carotenoid values within a relatively short time frame. Meinke et al. [28] showed an increase in both skin and blood carotenoids by comparing the effects of an oil extract rich in various carotenoids to those of a placebo oil. All these studies clearly indicate that providing relatively bioavailable carotenoids through supplementation impacts skin carotenoid status . In another double blind placebo controlled study performed with 24 healthy volunteers Meinke et al. [28] supplemented the volunteer’s diet with a natural carotenoid-rich product (BioActive Food GmbH, Bad Segeberg, Germany) containing curly kale extract, sea-buckthorn oil and olive oil.
Regarding food-based interventions Mayne et al. [3] report that an analysis of their early survey of 1375 healthy subjects indicated a pronounced cross-sectional relationship between self-reported fruit and vegetable intake (a source of carotenoids) and skin carotenoids RRS status [5, 4]. Subsequent cross-sectional studies are also quite consistent in showing significant associations between self – reported consumption of fruits/vegetables and/or dietary carotenoid intake and skin carotenoid status. This has been observed both in adults [29, 3, 30, 31] and in children [32]. It has been shown that skin carotenoid levels decreased during depletion and increased during high-carotenoid feeding, with skin carotenoid status tracking similarly to plasma carotenoids although the rates of decrease (during depletion) were faster in plasma versus skin. Skin carotenoids had not yet plateaued by 8 weeks post-intervention, suggesting that they reflect intake over at least the prior 2+ months. [3] Similar results were obtained by Jahns et al. [33], comparing RRS results with plasma HPLC analysis (see Figure 16). Twenty-nine participants consumed low-carotenoid diets (6 weeks, phases 1 and 3), a provided diet containing 6-cup equivalents (1046g/d) of vegetables and fruit (8 weeks, phase 2) and their usual diet (final 8 weeks, phase 4). Skin carotenoid status was measures by RRS >= 2 times per week during phases 1, 3 and 4 and 5 times per week during phase 2. At baseline, skin and plasma total carotenoid values were correlated (r=0.61, P<0.001). Skin and plasma carotenoid values decreased 36% and 30%, respectively, from baseline to the end of phase 1 and then increased by >200% at the end of phase 2. Plasma carotenoids returned to baseline concentrations by the middle of phase 3 and skin carotenoid concentrations by the middle of phase 4.
Thus multiple lines of evidence now show that skin carotenoid status is responsive to carotenoid intervention involving supplements, vegetable oil extracts given as dietary supplements and carotenoid-rich fruits and vegetables as food-based interventions. [3]
Smoking
Meinke et al. [69] report that the carotenoid levels in skin of smokers are significantly low er, on average by 21% for total carotenoids, than in non-smokers. Mayne et al. [3] report that an analysis of their early survey of 1375 healthy subjects revealed that smokers had much lower levels of sk in carotenoids than non-smokers [5, 4]. This has subsequently been observed in other studies [29]. More specifically, smokers had a 20-30% reduction in skin carotenoid levels when compar ed to non- smokers. This is due to the direct effects of smoking and the fact that smokers are additionally prone to lower intake of carotenoids. Scarmo et al. [34] showed that carotenoid levels in children, having a smoker in the home, were also associated with a modest reduction (7%). Ermakov et al. [5] show data of a 30% decrease of skin carotenoid levels in smokers compared to non -smokers (see Figure 4).
![Figure 4: Resonance Raman intensity (counts) in nonsmokers and cigarette smokers, showing ~30% decrease of skin carotenoid levels in smokers [29]](http://blog.one-x.co/wp-content/uploads/2016/09/onex3pic.png)
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