Ultraviolet (UV) radiation from the sun is a potent environmental factor with profound effects on skin cells.

While natural exposure is necessary for vital processes like vitamin D synthesis, excessive or unprotected UV radiation leads to a spectrum of cellular alterations ranging from DNA damage and oxidative stress to inflammation and premature aging.

Types of UV Radiation

Ultraviolet (UV) radiation is classified into three main bands: UVA (≈ 315–400 nm), UVB (≈ 280–315 nm), and UVC (≈ 100–280 nm). Fortunately, natural UVC is completely absorbed by the Earth’s atmosphere and does not reach the skin. The UVA portion that does reach the surface penetrates deeply into the dermal layers and contributes to oxidative stress and long-term skin damage via the generation of reactive oxygen species (ROS). Meanwhile, UVB — more energetic per photon — primarily affects the outer epidermis and is absorbed directly by DNA, forming photoproducts like cyclobutane‑pyrimidine dimers; this DNA damage underlies risks such as sunburn, premature aging, and skin cancer.

DNA Damage and Cellular Repair Mechanisms

UVB radiation induces characteristic damage like cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts that distort the DNA helix. These lesions interfere with replication and transcription and can result in mutagenesis—a principal factor in skin cancer development.

Keratinocytes—the predominant cell type in the outer skin layer—respond to UV-induced DNA damage by activating repair pathways. If damage overwhelms repair, cells may go through apoptosis to prevent propagation of mutations, often observed clinically as sunburn cells.

However, chronic UV exposure impairs repair efficiency and may induce immunosuppression by altering the function of Langerhans cells, the skin's antigen-presenting immune cells. This immunosuppression fosters an environment conducive to tumor growth and progression.

Oxidative Stress and Inflammation

UVA-driven ROS generation attacks cellular components including lipids, proteins, and nucleic acids, disrupting membrane integrity and cellular homeostasis. This oxidative stress activates signal transduction pathways involving epidermal growth factor and tumor necrosis factor, resulting in increased production of pro-inflammatory mediators such as prostaglandins and cytokines.

These inflammatory reactions manifest as erythema, heat, and pain during sunburn. Prolonged inflammation also accelerates photoaging—characterized by skin wrinkling, sagging, and pigmentation irregularities—through degradation of collagen and extracellular matrix components.

Skin Defense Strategies: Melanin and Hyperplasia

Melanin, produced by melanocytes, acts as a natural photoprotective pigment by absorbing and dissipating UV radiation. Its synthesis increases upon UV exposure, giving rise to tanning as a defensive response. Melanin reduces the formation of DNA lesions and ROS, mitigating UV-induced damage.

Additionally, repeated UV exposure triggers epidermal hyperplasia—a thickening of the outer skin layer accomplished by increased keratinocyte proliferation. This response enhances the skin’s physical barrier, reducing UV and potential injury.

According to a review by D’Orazio, Jarrett, Amaro‑Ortiz and Scott, published in International Journal of Molecular Sciences, UV radiation — especially UVB radiation — induces characteristic DNA damage in skin cells by forming lesions such as cyclobutane pyrimidine dimers (CPDs) and 6‑4 photoproducts (6‑4PPs), which distort the DNA helix, interfere with replication and transcription, and significantly elevate the risk of mutagenesis and skin cancer.

UV radiation impacts skin cells through direct DNA damage, oxidative stress, and inflammation, which together contribute to acute effects like sunburn and long-term consequences such as photoaging and carcinogenesis. The interplay between UVA and UVB rays influences distinct but overlapping cellular pathways. Natural defense mechanisms including melanin production and epidermal thickening provide protection but are insufficient against excessive exposure.