Fitzpatrick skin type patients. A botanical extract, Fernblock®, obtained from the tropical plant Polypodium leucotomos, is a potent antioxidant and has shown to protect against damaged induced by visible light. Taken orally, Fernblock has shown to be effective in reducing visible light induced pigmentation.2 Regarding infrared light, 50% of the electromagnetic energy reaching the earth is infrared with infrared A (IRA) accounting for about one third of the electromagnetic energy. Infrared can penetrate the skin producing an increase in skin temperature and activating mitochondrial reactive oxygen species (ROS) via up-regulation of MMP-1, MMP-3, and MMP-13. This results in collagen destruction accounting for the coarse wrinkling seen in human skin exposed to repeated high temperature. There are generally few active ingredients that shield against IRA although some antioxidants have been demonstrated orally and/or topically to help protect against IRA-induced ROS production and MMP-1 expression.
A new form of light injury, known as digital light pollution or high energy visible light damage, is blue light (412–426 nm) at high fluence.3 Porphyrin-containing enzymes and flavoproteins are thought to be the photoreceptors for blue light damaging the mitochondrial respiratory chain. Computer screens, cell phones, and other digital devices produce this light. Opaque blocking agents, such as pigments, charcoal, red algae, and the Polypodium leucotomos extract before mentioned, are being incorporated into skin care products to prevent the blue light from reaching and damaging the skin. In addition to electromagnetic radiation impacting the skin, pollutants found in the air can also generate ROS and prematurely age the skin. Most of the damaging pollution contains nanoparticles generated by combustion. This includes the smoking of tobacco products where the burning of the plant material creates highly energetic nanoparticles that damage the skin. Air pollution from internal combustion engines or factory exhaust also contains nanoparticles that damage the skin. One method to minimize skin damage from aerosolized nanoparticles is to prevent them from touching the skin, which can be achieved by wearing a sunscreen, moisturizer, or facial foundation. Pollutants can also damage skin by activating Aryl hydrocarbon receptors (AhR), which trigger hyperpigmentation, MMP-1 expression, and damage to keratinocytes. Inhibition of the activation of AhR by ingredients such as the extract of Deschampsia antarctica has been shown to protect against morphological alterations to skin structure and prevent DNA damage induced by pollutants in a human skin model. It also helps to enhance the skin barrier function by increasing the production of loricrin.4,5 Deschampsia antarctica is an extremophile plant that grows in the Antarctic in an environment characterized by very low temperatures, high oxygen concentrations, high salinity, and intense solar radiation.
Another approach to minimizing problems associated with ROS induced skin damage is the use of topical and/or oral antioxidants. Antioxidants must be considered inactive ingredients, as they are not listed on the sunscreen monograph and cannot be claimed as photoprotectors. Antioxidants are incorporated into some sunscreens because of their ability to scavenge and reduce ROS levels and may suppress ROS formation by 2.4-fold in SPF 15 formulations. Ingredients that are used for this purpose include retinol, ascorbic acid, alpha-tocopherol, and green tea polyphenols, among others, but they must be stabilized in formulation, so they do not undergo oxidation.6 Prevention of DNA damage from ROS is minimized, but not eliminated, through the use of sunscreens and antioxidants. Another functional target for cosmeceuticals is DNA repair. Nicotinamide (amide form of vitamin B3) prevents the UV-induced ATP depletion boosting cellular energy and enhances DNA repair activity.7 Fernblock has been demonstrated to induce and accelerate repair of DNA damage, by reducing and preventing the formation of cyclobutane pyrimidine dimers (CPD) and 8-oxo-dGuanine caused by UV exposure.8 DNA repair enzymes, such as endonucleases, glycosylases, and photolyases, have been developed.9 The T4 endonuclease V recognizes CPD and repairs DNA by catalyzing glycosylase to release thymine and then uses AP lyase to incise the phosphodiester backbone at the site of the missing base to cause a single-stranded break. The cell then supplies exonuclease to remove the base and then polymerase fills the gap thus repairing the DNA. Photolyases are not found in mammalian cells but are used for DNA repair in bacteria and plants. This mechanism uses blue light to repair DNA by catalyzing a reaction that transfers electrons which split the cyclobutane ring in the damaged DNA.10 DNA repair enzymes can be delivered to the skin in liposomes with a diameter of about 150 nm.
Another new concept in protection and repair is the composition of the microbiome, the bacterial flora that covers the entire skin surface representing the collective genome of the indigenous microorganisms colonizing the whole body.11 While the “normal” microbiome has not been confirmed, it is known that it varies by sex, age, body location, and immune status. UV radiation can induce skin microbiome alteration.12 Skin care products have been developed based on prebiotic, probiotic, and postbiotic principles. Prebiotic skin care contains ingredients that are able to encourage the growth of microbiome organisms while probiotic skin care contains either live bacteria, requiring refrigeration of the product, or ultrasound-inactivated bacterial extracts. Postbiotic products contain non-viable bacterial products or metabolic by-products from postbiotic bacteria, such as enzymes, peptides, peptidoglycan-derived muropeptides, polysaccharides, cell surface proteins, etc. Some skin care companies are now testing their formulations to ensure they do not cause microbiome damage making the claim “microbiome friendly” or “microbiome neutral.” However, more research is needed in the area of microbiome protection.
A new form of light injury, known as digital light pollution or high energy visible light damage, is blue light (412–426 nm) at high fluence.3 Porphyrin-containing enzymes and flavoproteins are thought to be the photoreceptors for blue light damaging the mitochondrial respiratory chain. Computer screens, cell phones, and other digital devices produce this light. Opaque blocking agents, such as pigments, charcoal, red algae, and the Polypodium leucotomos extract before mentioned, are being incorporated into skin care products to prevent the blue light from reaching and damaging the skin. In addition to electromagnetic radiation impacting the skin, pollutants found in the air can also generate ROS and prematurely age the skin. Most of the damaging pollution contains nanoparticles generated by combustion. This includes the smoking of tobacco products where the burning of the plant material creates highly energetic nanoparticles that damage the skin. Air pollution from internal combustion engines or factory exhaust also contains nanoparticles that damage the skin. One method to minimize skin damage from aerosolized nanoparticles is to prevent them from touching the skin, which can be achieved by wearing a sunscreen, moisturizer, or facial foundation. Pollutants can also damage skin by activating Aryl hydrocarbon receptors (AhR), which trigger hyperpigmentation, MMP-1 expression, and damage to keratinocytes. Inhibition of the activation of AhR by ingredients such as the extract of Deschampsia antarctica has been shown to protect against morphological alterations to skin structure and prevent DNA damage induced by pollutants in a human skin model. It also helps to enhance the skin barrier function by increasing the production of loricrin.4,5 Deschampsia antarctica is an extremophile plant that grows in the Antarctic in an environment characterized by very low temperatures, high oxygen concentrations, high salinity, and intense solar radiation.
Another approach to minimizing problems associated with ROS induced skin damage is the use of topical and/or oral antioxidants. Antioxidants must be considered inactive ingredients, as they are not listed on the sunscreen monograph and cannot be claimed as photoprotectors. Antioxidants are incorporated into some sunscreens because of their ability to scavenge and reduce ROS levels and may suppress ROS formation by 2.4-fold in SPF 15 formulations. Ingredients that are used for this purpose include retinol, ascorbic acid, alpha-tocopherol, and green tea polyphenols, among others, but they must be stabilized in formulation, so they do not undergo oxidation.6 Prevention of DNA damage from ROS is minimized, but not eliminated, through the use of sunscreens and antioxidants. Another functional target for cosmeceuticals is DNA repair. Nicotinamide (amide form of vitamin B3) prevents the UV-induced ATP depletion boosting cellular energy and enhances DNA repair activity.7 Fernblock has been demonstrated to induce and accelerate repair of DNA damage, by reducing and preventing the formation of cyclobutane pyrimidine dimers (CPD) and 8-oxo-dGuanine caused by UV exposure.8 DNA repair enzymes, such as endonucleases, glycosylases, and photolyases, have been developed.9 The T4 endonuclease V recognizes CPD and repairs DNA by catalyzing glycosylase to release thymine and then uses AP lyase to incise the phosphodiester backbone at the site of the missing base to cause a single-stranded break. The cell then supplies exonuclease to remove the base and then polymerase fills the gap thus repairing the DNA. Photolyases are not found in mammalian cells but are used for DNA repair in bacteria and plants. This mechanism uses blue light to repair DNA by catalyzing a reaction that transfers electrons which split the cyclobutane ring in the damaged DNA.10 DNA repair enzymes can be delivered to the skin in liposomes with a diameter of about 150 nm.
Another new concept in protection and repair is the composition of the microbiome, the bacterial flora that covers the entire skin surface representing the collective genome of the indigenous microorganisms colonizing the whole body.11 While the “normal” microbiome has not been confirmed, it is known that it varies by sex, age, body location, and immune status. UV radiation can induce skin microbiome alteration.12 Skin care products have been developed based on prebiotic, probiotic, and postbiotic principles. Prebiotic skin care contains ingredients that are able to encourage the growth of microbiome organisms while probiotic skin care contains either live bacteria, requiring refrigeration of the product, or ultrasound-inactivated bacterial extracts. Postbiotic products contain non-viable bacterial products or metabolic by-products from postbiotic bacteria, such as enzymes, peptides, peptidoglycan-derived muropeptides, polysaccharides, cell surface proteins, etc. Some skin care companies are now testing their formulations to ensure they do not cause microbiome damage making the claim “microbiome friendly” or “microbiome neutral.” However, more research is needed in the area of microbiome protection.
