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Ultraviolet (UV) radiation, comprising UVA (320–400 nm) and UVB (280–320 nm), is a physical agent rather than a biological molecule or receptor [1]. UVB radiation is primarily responsible for direct DNA damage, such as the formation of cyclobutane pyrimidine dimers, and is the main cause of sunburn (erythema) [2, 3]. UVA radiation penetrates deeper into the skin, generating reactive oxygen species that lead to indirect oxidative damage and photoaging [3]. While UV exposure is necessary for Vitamin D synthesis, chronic exposure is a major risk factor for skin cancers, including melanoma and basal cell carcinoma [1, 2]. In a pharmacological context, UV radiation is the target of photoprotective agents like sunscreens, which absorb or reflect photons to prevent tissue damage [4]. Additionally, UV radiation is used therapeutically in PUVA (Psoralen plus UVA) therapy to treat conditions like psoriasis by inducing DNA cross-linking in hyperproliferative cells [5].
Sunscreens act as physical or chemical filters that absorb or reflect UV photons to prevent them from reaching the skin's cellular DNA [3, 4]. In PUVA therapy, psoralens like methoxsalen intercalate into DNA and form cross-links upon UVA activation, inhibiting DNA synthesis and cell division [5].
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