Oxidatively Generated Damage to Cellular <scp>DNA</scp> by <scp>UVB</scp> and <scp>UVA</scp> Radiation^,

<jats:title>Abstract</jats:title><jats:p>This review article focuses on a critical survey of the main available information on the <jats:styled-content style="fixed-case">UVB</jats:styled-content> and <jats:styled-content style="fixed-case">UVA</jats:styled-content> oxidative reactions to cellular <jats:styled-content style="fixed-case">DNA</jats:styled-content> as the result of direct interactions of <jats:styled-content style="fixed-case">UV</jats:styled-content> photons, photosensitized pathways and biochemical responses including inflammation and bystander effects. <jats:styled-content style="fixed-case">UVA</jats:styled-content> radiation appears to be much more efficient than <jats:styled-content style="fixed-case">UVB</jats:styled-content> in inducing oxidatively generated damage to the bases and 2‐deoxyribose moieties of <jats:styled-content style="fixed-case">DNA</jats:styled-content> in isolated cells and skin. The <jats:styled-content style="fixed-case">UVA</jats:styled-content>‐induced generation of 8‐oxo‐7,8‐dihydroguanine is mostly rationalized in terms of selective guanine oxidation by singlet oxygen generated through type <jats:styled-content style="fixed-case">II</jats:styled-content> photosensitization mechanism. In addition, hydroxyl radical whose formation may be accounted for by metal‐catalyzed Haber–Weiss reactions subsequent to the initial generation of superoxide anion radical contributes in a minor way to the <jats:styled-content style="fixed-case">DNA</jats:styled-content> degradation. This leads to the formation of both oxidized purine and pyrimidine bases together with <jats:styled-content style="fixed-case">DNA</jats:styled-content> single‐strand breaks at the exclusion, however, of direct double‐strand breaks. No evidence has been provided so far for the implication of delayed oxidative degradation pathways of cellular <jats:styled-content style="fixed-case">DNA</jats:styled-content>. In that respect putative characteristic <jats:styled-content style="fixed-case">UVA</jats:styled-content>‐induced <jats:styled-content style="fixed-case">DNA</jats:styled-content> damage could include single and more complex lesions arising from one‐electron oxidation of the guanine base together with aldehyde adducts to amino‐substituted nucleobases.</jats:p>