title: Skin damage and mitochondrial dysfunction after acute ultraviolet B irradiation: relationship with nitric oxide production.
abstract: BACKGROUND
  Ultraviolet (UV) radiation is the main environmental carcinogen. It is able to induce injury in the keratinocytes, which triggers mechanisms in order to protect the skin against molecular alterations that may lead to the development of skin cancer. UVB is capable of producing genotoxic damage, directly or indirectly through reactive oxygen species, inducing DNA alterations and mutations. UVB radiation has also been associated with the generation of nitric oxide (NO), which is able to induce many physiological and physiopathological processes. The aim of the current study was to investigate the effect of UVB irradiation in hairless mice skin.
  
  
  METHODS
  We evaluated the effect of an acute dose (200 mJ/cm(2)) of UVB irradiation correlating with histological alterations, nitric oxide synthase expression and activity, mitochondrial respiratory function, superoxide anion production and lipid peroxidation, 0, 6, 17 and 24 h post-irradiation treatment.
  
  
  RESULTS
  Morphological analysis showed disruption of the epidermal stratum corneum and basale after UVB irradiation. The results indicated that skin UVB irradiation was associated with an increased cytosolic inducible nitric oxide synthase (iNOS) expression, inversely related to lipid peroxidation processes. An increase in mitochondrial superoxide anion (O(2) (*-)) and NO production 17 h post-irradiation was correlated with a mitochondrial dysfunction, all of them integrating the skin response to acute UVB irradiation.
  
  
  CONCLUSIONS
  UVB irradiation of the skin produces morphological alterations as a consequence of the induction of molecular mechanisms associated with mitochondrial respiratory dysfunction and O(2) (*-) production, probably mediated by the increased mitochondrial NO production. On the other hand lipid peroxidation decrease inversely correlates with cytosolic iNOS expression, suggesting a protective role for the inflammatory response.
authors.affiliation: Institute of Immunology, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina. danielgm@ffyb.uba.ar
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Gonzalez Maglio
authors.forename: Mariela L
authors.initials: ML
authors.lastname: Paz
authors.forename: Alejandro
authors.initials: A
authors.lastname: Ferrari
authors.forename: Federico S
authors.initials: FS
authors.lastname: Weill
authors.forename: Analía
authors.initials: A
authors.lastname: Czerniczyniec
authors.forename: Juliana
authors.initials: J
authors.lastname: Leoni
authors.forename: Juanita
authors.initials: J
authors.lastname: Bustamante
mesh_terms: D000818:Animals; D005260:Female; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000528:radiation effects*; D008297:Male; D051379:Mice; D008812:Mice, Hairless; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D009569:Nitric Oxide / Q000096:biosynthesis*; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D012867:Skin / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D012871:Skin Diseases / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D013481:Superoxides / Q000378:metabolism*; D013997:Time Factors; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D013481:Superoxides; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II