Solar ultraviolet (UV) radiation is an important risk factor in skin carcinogenesis. This has been attributed mainly to the UVB waveband because the high-energetic photons are capable of interacting with DNA and inducing DNA damage. Recently, UVA light has also gained increasing interest in relation to DNA alteration. Although UVA photons are less energetic than UVB, they comprise a major fraction of sunlight UV radiation and penetrate deep into the skin. The study was carried out to compare the acute effects of UVA and UVB light on SKH-1 mice in relation to DNA damage and associated parameters. Mice were exposed to UVA (10 and 20 J/cm(2)) or UVB (200 and 800 mJ/cm(2)) radiation. The number of DNA single-strand breaks (SSB) in lymphocytes, amount of phosphorylated histone H2AX (gamma-H2AX) and apoptosis or DNA fragmentation (TUNEL-positive cells) in skin sections and level of gamma-H2AX, activated caspase-3 and phosphorylated p53 in skin were evaluated after 4 and 24 h. SSB analyzed by alkaline comet assay were found to be 4 and 24 h following UVB and UVA treatment, respectively. TUNEL and gamma-H2AX-positive cell were observed only in UVB exposed animals at both time intervals. The level of activated caspase-3 and phospho-p53 was increased 24 h after UVA and UVB radiation and was more apparent in UVB treated mice. The results indicate that the mechanism of DNA damage caused by acute UVA exposure includes formation of SSB (oxidative damage), but not double-strand breaks.

Solar light is the main environmental factor implicated in various skin disorders. Extensive evidence supports the notion that the whole solar spectrum (UV, visible and infrared wavelengths) participates in skin cells damage.1) However, UV wavelengths are regarded as the most hazardous and most toxic. The sun is primarily a UVA source with an approximate terrestrial UVB content of about 5-10%. UVA (315-400 nm) penetrates deep into the skin. Approximately 80% of UVA reaches the dermal-epidermal junction and around 10% of UVA even reaches the hypodermis. UVA photons are less energetic than UVB and cause mainly indirect damage via increased generation of reactive oxygen and nitrogen species (RONS). These reactive species attack biomolecules resulting in several types of DNA damage (e.g. DNA single strand breaks, DNA interstrand cross-links and nucleotide base modifications), formation of oxidized fragments and products of lipids (e.g. lipid alkoxyl radicals, aldehydes, alkanes, lipid (hydro)peroxides and epoxides) and oxidatively modified proteins and saccharides. In contrast, incoming UVB (295-315 nm) is mostly absorbed by the epidermis (90%). UVB is directly absorbed by the aromatic heterocyclic bases of DNA. As a result of UVB photons absorption cyclobutane-pyrimidine dimers and pyrimidine-(6-4)-pyrimidone photoproducts are formed.2) Aromatic amino acids such as tryptophan and tyrosine also act as potent UVB radiation absorbers and their interaction with high energetic UVB photons leads to the generation of several derivatives. Of these, 6-formylindolo[3,2-b]carbazole (FICZ) has been recognized to have fundamental importance.3) Amino acid modification alters protein function as well as affects cellular signalling. However, the division between UVA and UVB is arbitrary and UVB participates in RONS production as well. 4)Skin cells are equipped with several non-enzymic (ascorbic acid, tocopherol, ubiquinol, and glutathione (GSH)) and enzymic antioxidants (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX)) that maintain the prooxidant/antioxidant balance by rapid RONS elimination, resulting in cell and tissue stabilization. However, flooding of reactive species causes antioxidants depletion and further formation of reactive products that both result in oxidative stress. Production of modified biomolecules is also accompanied by alteration to various enzyme activity and regulation of gene expression in several pathways such as inflammatory cytokines, mitogen-activated protein kinases, matrix metalloproteinases, nuclear factor-kB, nuclear factor erythroid-2 related factor 2 (Nrf2) and phase 2 detoxifying enzymes such as nicotinamide adenine dinucleotide (phosphate) quinone oxidoreductase (NQO1), hem oxygenase-1 (HO-1), glutathione transferase (GST) and glutathione reductase (GSR). 4,5) Over 50 years of UV light research, a number of authors have examined the effects of chronic and/or repeated exposures. However, lacking of number reports has pursued the acute effects of UVA/UVB exposure. [6][7][...

Background. Solar light generates inflammatory responses in exposed skin. These effects are generally attributed to UVB light. However, skin is exposed to a huge quantum of UVA photons as UVA is a predominant part of sunlight and the radiation used in tanning beds. We examined the effects of a single exposure to UVA and UVB wavebands on cytokine levels in skin and plasma, myeloperoxidase (MPO) activity, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) in skin. Methods. Hairless mice were irradiated with either UVA (10 or 20 J/cm 2 ) or UVB (200 or 800 mJ/cm 2 ). The effects were assessed after 4/24 h. Plasma cytokine levels were evaluated using a Bio-Plex cytokine assay. Cytokine, iNOS and COX-2 levels in skin were determined by Western blot. Skin MPO activity was monitored spectrophotometrically. Results. UVB induced up-regulation of interleukin-1β (IL-1β) and interleukin-6 (IL-6) and decrease in interleukin-10 (IL-10) mainly after 4 h. In contrast, UVA caused increase in levels of tumor necrosis factor-alpha (TNF-α) and IL-6 after 4 h and up-regulated IL-10 and interleukin-12 (IL-12) after 24 h. The increase in MPO activity from infiltrated leucocytes was observed only in UVB irradiated animals. iNOS was up-regulated 4 h after UVA and UVB treatment. No significant effect on COX-2 expression was detected. Conclusions. UVA and UVB light affected several inflammatory markers. For individual waveband, changes in plasma parameters did not correlate with those in skin. Thus evaluation of plasma samples cannot simply be replaced by determination in skin specimens and vice versa.