Photoprotection describes mechanisms that limit solar radiation’s effects on the body. Skin has natural defenses, but they are insufficient during intense or prolonged exposure. External—and sometimes internal—strategies are necessary to reinforce protection. What exactly does this involve? Learn more about internal and external photoprotection in this article.
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Sun: how to protect skin from the inside and the outside?
Summary
- What is internal photoprotection?
- Systemic photoprotection: how to enhance the skin’s natural protection?
- How to define external photoprotection?
- Sources
Published June 26, 2025,
updated on June 27, 2025,
by
Pauline, Chemical Engineer
—
14 min read
What is internal photoprotection?
Internal photoprotection relies on a set of mechanisms integrated into the skin’s structure and function.
It combines three main defense mechanisms: the stratum corneum’s physical barrier, pigmentation—with melanin—and the cellular DNA repair systems. These defenses vary in effectiveness by skin phototype, age, and body site but form the initial biological response to solar exposure.
The stratum corneum: the first physical barrier against sunlight.
The stratum corneum, the outermost layer of the epidermis, acts as a first barrier against solar radiation. It has a dual photoprotective role: the stratum corneum reflects part of the light in visible and infrared wavelengths and absorbs a fraction of UV. The effectiveness of this barrier in protecting the body from the sun varies significantly with its thickness, which differs across the body. Indeed, the stratum corneum on the sole of the foot measures about 1.5 mm, compared with less than 0.1 mm around the eye area. The photoprotective capacity of the stratum corneum also depends on phototype: it is higher in individuals with darker skin, due to the diffuse presence of melanin granules. Most UVB is blocked by the stratum corneum, unlike UVA, which penetrate more deeply.
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≈ 70%
UVB rays are blocked by the stratum corneum.
≈ 10%
UVB rays penetrate the dermis.
Melanin: a potent biological filter.
Melanin is the central component of internal photoprotection. Produced by melanocytes in the epidermis’s basal layer during the process of melanogenesis, it absorbs over 90% of UV rays that penetrate the stratum corneum. Melanin protects melanocytes and keratinocytes by neutralizing free radicals generated by photons and limiting DNA damage. Contrary to some beliefs, melanocyte numbers remain constant across individuals regardless of phototype, but melanosome size, density, and distribution—the organelles containing melanin—vary. In darker skin, melanosomes are larger and distributed throughout the epidermis up to the stratum corneum. This increases photoprotective capacity.
Skin melanin content by phototype.
Source: Hearing V. J., et al. The protective role of melanin against UV damage in human skin. Photochemistry and Photobiology (2007).
At the molecular level, melanin synthesis is regulated by a complex network of cellular signals. The key enzyme in this process is tyrosinase, which catalyzes the initial steps in converting tyrosine to melanin. Its activity is modulated by associated proteins, such as tyrosinase-related protein 1 (TRP1) and dopachrome tautomerase (DCT), both expressed by melanocytes. These pigment cells are also influenced by surrounding keratinocytes, which release paracrine signals, especially under UV exposure. A major hormonal regulator is melanocyte-stimulating hormone (MSH), which activates the MC1R receptor on the surface of melanocytes. This receptor directs synthesis toward eumelanin—a brown-black photoprotective pigment—or pheomelanin—a red-yellow pigment that is less efficient and potentially pro-oxidant under UV radiation. Genetic variations in the MC1R gene are responsible for specific phenotypes (very fair skin, freckles) and increased sun sensitivity.
Melanin biosynthesis pathways.
Source: Thesis by Zacharie SEGAOULA. Relevance and preclinical and clinical validations of the spontaneous canine melanoma model in therapeutic development in oncology (2017).
Cellular repair systems to correct UV-induced damage.
When UV rays penetrate skin layers, they interact with chromophores and generate reactive oxygen species and DNA photoproducts, including pyrimidine dimers. These changes can be mutagenic. In response, the skin activates several cellular repair systems to preserve genomic integrity. The photoreactivation mechanism, for example, uses an enzyme, photolyase, to restore thymine-thymine dimers under visible light. However, the efficiency of cellular repair pathways declines with age, increasing skin cancer risk in older individuals or those with high exposure.
Systemic photoprotection: how to enhance the skin’s natural protection?
Some molecules found in our diet or available as dietary supplements have shown a modest photoprotective effect in research. However, the magnitude of this effect, its duration, and above all its clinical significance remain under debate. While a varied, balanced diet is recommended, we advise consulting a physician before starting supplementation.
Vitamins C and E: a moderate photoprotective synergy.
Individually, neither vitamin C (ascorbic acid) nor vitamin E (α-tocopherol) has shown a convincing photoprotective effect in vivo. However, their oral combination appears to induce a slight increase in the minimal erythema dose (MED), indicating enhanced skin resistance to UVB rays. Three controlled studies reported a modest but significant increase in MED, ranging from 16.5 to 80 mJ/cm2, attributed to vitamin C’s ability to regenerate oxidized vitamin E within cell membranes. For example, one of these studies involved 45 volunteers with phototypes II to IV divided into three groups. Over one week, the first group received 805 mg of α-tocopherol daily, the second received 2 g of ascorbic acid, and the third received 805 mg of α-tocopherol plus 2 g of ascorbic acid. The following results showed a slight MED increase in groups 1 and 3.
| Measurement | Group 1 (vitamin E) | Group 2 (vitamin C) | Group 3 (vitamin C + vitamin E) |
|---|---|---|---|
| Before MED | 60 mJ/cm2 | 60 mJ/cm2 | 50 mJ/cm2 |
| After MED | 65 mJ/cm2 | 60 mJ/cm2 | 70 mJ/cm2 |
MED before and after one week of vitamin C and/or vitamin E supplementation.
Source: Cortes-Franco R et al. UVB photoprotection with antioxidants: effects of oral therapy with d-alpha-tocopherol and ascorbic acid on the minimal erythema dose. Acta Dermato-Venereologica. 2002.
Carotenoids: a protective antioxidant role.
Carotenoids such as lycopene, lutein, zeaxanthin, and provitamin A compounds like β-carotene occur naturally in fruits and vegetables. They accumulate in the epidermis, where they scavenge free radicals and protect cellular structures from UV damage. β-carotene is the most studied carotenoid. Its protective effect was first observed in the 1970s in patients with erythropoietic protoporphyria, a rare genetic disorder that causes skin photosensitivity among other symptoms. In healthy individuals, results are more mixed. Some studies report a modest reduction in minimal erythema dose (MED), but only after six weeks of continuous supplementation at doses above 10 mg/day.
Regarding lycopene, another carotenoid, two clinical studies explored its effect on UVB-induced erythema. In the first, 11 participants received tomato concentrate containing 16 mg of lycopene for 10 weeks. After that, a 40% reduction in erythema on the back of the hand following MED irradiation was observed. In the second study, 36 volunteers were randomized to receive synthetic lycopene, tomato extract, or a lycopene beverage for 12 weeks. All three forms resulted in modest increases in skin lycopene levels and reduced erythema by 38 to 48%. Further research is needed, but lycopene appears to be a promising antioxidant for skin protection.
Nicotinamide: a photoprotective vitamin.
Nicotinamide, or niacinamide, is a precursor of NAD+, a cofactor essential for DNA repair and post-UV immune response. Unlike other vitamins, its photoprotective effects have been assessed in several clinical trials with promising results. A phase III double-blind randomized study enrolled nearly 400 participants who had at least two nonmelanoma skin cancers (basal cell or squamous cell carcinoma) in the past five years. They received 500 mg of nicotinamide twice daily for 12 months or a placebo.
At the end of one year, the nicotinamide group showed a significant 23% reduction in new nonmelanoma skin cancer cases compared with the placebo group. The number of actinic keratoses, precancerous lesions, also decreased significantly by the third month. However, the benefits did not persist after supplementation stopped.
How to define external photoprotection?
External photoprotection includes clothing-based photoprotection and sunscreen application. External photoprotection is often regarded as the cornerstone of sun protection.
Clothing: a primary physical barrier.
A garment can provide an effective physical barrier against UV. To assess this protection, an index was defined: the ultraviolet protection factor (UPF). A higher value indicates that the fabric blocks UVB and UVA. A textile’s UV filtering ability depends on fiber type, weave density, thickness, color, moisture, and wear. For example, dark denim can reach UPF 50 and protect the skin, while a thin white cotton t-shirt may only reach 7 to 10. UPF is regulated by the international standard AS/NZS 4399.
| UPF rating from 0 to 15 | UPF rating from 15 to 24 | UPF rating of 25 to 39 | UPF rating of 40 or higher |
|---|---|---|---|
| The garment does not block UV radiation. | The garment provides moderate protection and filters between 93% and 95% of UV rays. | The garment offers good protection and filters between 96% and 97.4% of UV rays. | The garment provides high protection and filters 97% to 98% of UV radiation. |
Protection levels ensured by UPF ratings.
Sun protection products: essentials for protecting skin from sun exposure.
Sun protection products – whether sticks, mists, sprays, lotions, or creams – represent a key strategy to protect skin from sun exposure. Their efficacy depends on the organic and/or mineral filters they contain. These molecules absorb and reflect UV rays, protecting skin from harmful effects. Sunscreen performance is measured by the SPF (Sun Protection Factor) and the UVA-PF (UVA protection factor), values measured duringrigorous laboratory and regulated evaluations. According to European regulations, a sunscreen must offer UVA protection amounting to at least one third of the UVB protection stated on the label.
The SPF measures protection against erythemal UV (85% UVB and 15% UVA-II), responsible for sunburn, while the FP-UVA quantifies protection against UVA, which penetrates deeper into the skin and accelerates skin aging.
| Protection level | SPF measured in vivo | SPF indicated on the label | UVA-PF measured in vivo | UVA-PF claimed on the label |
|---|---|---|---|---|
| Low protection | 4 - 14,9 | 4, 6, 10 | 2 à 4 | PA+ |
| Medium protection | 15 - 29,9 | 15, 20, 25 | 4 à 8 | PA++ |
| High protection | 30 - 59,9 | 30, 50 | 8 à 12 | PA+++ |
| Very high protection | ≥ 60 | 50+ | > 12 | PA++++ |
Sunscreen categories based on SPF and UVA protection factor.
Source: Australian Government - Department of Health and Aged Care. Australian Regulatory Guidelines for Sunscreens (2023).
In practice, the effectiveness of a sunscreen product largely depends on the applied amount. While SPF tests use 2 mg/cm2, users apply one quarter of that (≈ 0.5 mg/cm2), which reduces actual protection. To reach the labeled protection, apply 2.5 finger widths of sunscreen to face and neck, eight to torso and back, four to each arm, one to each hand, six to each leg, and two to each foot.
Moreover, the application frequency of sunscreen is essential for prolonged exposure. If you spend the day in the sun, remember to reapply your sunscreen at least every two hours. Most UV filters degrade over time, reducing skin protection.
Sources
CORTES-FRANCO R. & al. UVB photoprotection with antioxidants: effects of oral therapy with d-alpha-tocopherol and ascorbic acid on the minimal erythema dose. Acta dermato-venereologica (2002).
LACOUR J.-P. & BÉANI J.-C. Photoprotection naturelle, photoprotection externe (topique et vestimentaire). Annales de Dermatologie et de Vénéréologie (2007).
HEARING V. J. & al. The protective role of melanin against UV damage in human skin. Photochemistry and Photobiology (2007).
COIFFARD L. J. M. & al. In vitro UV-A protection factor (PF-UVA) of organic and inorganic sunscreens. Pharmaceutical Development and Technology (2009).
ASKARIAN-AMIRI M. E. & al. Signaling pathways in
melanogenesis. International Journal of Molecular Sciences (2016).Thèse de Zacharie SEGAOULA. Pertinence et validations préclinique et clinique du modèle spontané canin de mélanome dans le développement thérapeutique en oncologie (2017).
TALVAS J. & VASSON M.-P. Photoprotection solaire interne et externe. Pratiques en Nutrition (2018).
ADLER B. & al. Systemic photoprotection. Current Dermatology Reports (2020).
Australian Government - Department of Health and Aged Care. Australian regulatory guidelines for sunscreens (2023).
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