The effects of the sun on the skin are a constant concern in dermatology and cosmetics. Although moderate sun exposure has physiological benefits, such as vitamin D synthesis, excessive and cumulative exposure can trigger profound alterations in the structure and function of the skin.
The human skin, as a barrier organ, is exposed daily to different types of electromagnetic radiation from the sun: ultraviolet (UV), visible (VIS), and infrared (IR). Each of them causes a different biological impact, contributing to photoaging, chronic inflammation, and even the development of skin cancer. Understanding the mechanisms through which these effects occur, and how to prevent them through effective cosmetic strategies, is key to preserving skin health in the long term.
Types of solar radiation
The electromagnetic spectrum emitted by the sun is divided into three main bands that reach the Earth’s surface: ultraviolet (UV), visible (VIS), and infrared (IR). Each of these bands has a different wavelength and energy level, which determines the depth of penetration into the skin and the biological effects it triggers.
Ultraviolet radiation represents only between 3% and 7% of the total solar radiation that reaches the Earth’s surface, but it has a high biological impact. It is subdivided into three types: UVC (100–280 nm), UVB (280–315 nm), and UVA (315–400 nm). UVC is almost completely filtered by the ozone layer, so the most relevant harmful effects come from UVB and UVA.
- UVB: It is responsible for the production of solar erythema and the direct formation of thymine dimers in DNA. It has limited penetration into the epidermis, but its high energy makes it one of the main causes of skin mutations.
- UVA: Although it has lower energy than UVB, it penetrates deeper, reaching the dermis. It acts mainly by generating free radicals that promote oxidative stress, chronic inflammation, and the degradation of the extracellular matrix.
- Visible light: It constitutes 44% of solar radiation. The blue-violet fraction (400–500 nm) has effects similar to UVA in terms of generating reactive oxygen species (ROS). In darker skin, it has been observed to induce long-lasting hyperpigmentation.
- Infrared (IR): It represents up to 53% of total solar radiation. The IR-A fraction (700–1400 nm) penetrates into the hypodermis and is associated with the activation of thermal receptors such as TRPV1, mitochondrial stress, and the activation of catabolic pathways such as the production of metalloproteinases.
Molecular mechanisms of solar damageMecanismos moleculares del daño solar
When the skin is exposed to the sun, a complex series of biological responses is triggered, mediated by the interaction of radiation with specific cellular components. These mechanisms not only explain acute damage, such as sunburn, but also cumulative chronic effects that impair the barrier function, tissue architecture, and genetic stability of the skin.
One of the key mechanisms is the generation of reactive oxygen species (ROS), such as hydrogen peroxide or the superoxide anion. These molecules are produced when UVA radiation, blue light, or infrared excite skin chromophores such as melanin, flavins, or cytochromes. ROS oxidize lipids, structural proteins such as collagen, and DNA components, leading to cellular dysfunction and tissue degradation.
In addition, UVB radiation produces direct DNA damage through the formation of pyrimidine dimers (CPDs and 6-4 PPs). If this damage is not effectively repaired by mechanisms such as nucleotide excision repair (NER), mutations accumulate that can lead to oncogenic transformations.
A disruption of cutaneous immune homeostasis has also been described. Continuous sun exposure decreases the density and functionality of Langerhans cells, which promotes a suppressed local immune response, weakening surveillance against abnormal cells or infections.
Finally, infrared A (IR-A) alters mitochondrial function in dermal fibroblasts. Dysfunction in the respiratory chain generates retrograde signals that activate nuclear transcription factors involved in inflammation (such as NF-κB), expression of MMPs (metalloproteinases), and a reduction in collagen synthesis.
Effects of the sun on the skin: clinical and visible consequences
The clinical effects of cumulative sun exposure can be divided into four main categories:
- Photoaging: It manifests as deep wrinkles, sagging, epidermal thickening, dermal elastosis, and pigment spots. It results from structural damage to collagen, elastin, and hyaluronic acid, as well as from the increase of degradative enzymes such as MMPs.
- Hyperpigmentations: These include solar lentigines, melasma, and post-inflammatory dyschromia. They are produced by direct or indirect activation of melanogenesis, especially after exposure to UVA and visible light in higher phototypes.
- Light-induced dermatoses: Some people develop exacerbated immune reactions such as chronic actinic dermatitis, polymorphic light eruption, or solar urticaria.
- Skin cancer: Basal cell carcinoma, squamous cell carcinoma, and melanoma are directly associated with accumulated UV radiation damage. The presence of mutations such as BRAF, p53, or defects in repair genes such as XPC or MC1R increases individual risk.
How to protect the skin from the sun: filters, antioxidants, and repair
Modern cosmetics have evolved from mere UV protection to comprehensive defense that addresses the entire solar spectrum and the molecular mechanisms involved.
- Sunscreens: Nowadays, chemical, physical, and pigmentary filters are combined to provide broad-spectrum protection. Mineral filters such as zinc oxide protect against UVA/UVB and, in pigmented formulations with iron oxides, also against visible light.
- Antioxidants: Ingredients such as vitamin C, vitamin E, ferulic acid, niacinamide, and resveratrol neutralize ROS and stabilize the skin barrier. The combination of these actives with sunscreens increases photoprotective efficacy and prevents deep oxidative damage.
- Cellular repair agents: Encapsulated enzymes contribute to the repair of DNA damaged after sun exposure. Extracts such as Centella asiatica are also used to modulate the post-UV inflammatory response.
- Active ingredients modulating specific pathways: Ingredients capable of inhibiting signaling via AhR, TRPV1, or NF-κB are being studied for their ability to prevent or reverse the epigenetic and pro-inflammatory effects of accumulated sun damage.
Conclusion
Exposure to solar radiation involves a complex interaction between different wavelengths and skin structures. Beyond sunburn, ultraviolet, visible, and infrared radiation generate a pro-oxidant and inflammatory environment that progressively deteriorates skin integrity. Understanding these mechanisms is key to developing effective protection and repair strategies. In this context, modern cosmetics must meet the challenge of offering comprehensive solutions that not only block radiation but also act at the molecular level to protect, repair, and prevent. The cosmetic science of the future no longer focuses solely on sunscreens, but on bioactive ingredients that modulate critical cellular pathways to preserve skin health.
Do you formulate products to protect the skin from the sun? At Ismael Quesada Personal Care, we select ingredients that address sun damage from its origin. Contact us to discover multifunctional actives and technical solutions for your next sun care line.