INVESTIGADORES
GONZALEZ MAGLIO Daniel Horacio
artículos
Título:
Skin damage and mitochondrial dysfunction after acute UVB irradiation: relationship with nitric oxide production
Autor/es:
DANIEL H. GONZALEZ MAGLIO; MARIELA L. PAZ; ALEJANDRO FERRARI; FEDERICO S. WEILL; ANALÍA CZERNICZYNIEC; JULIANA LEONI; JUANITA BUSTAMANTE
Revista:
PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE
Editorial:
Blackwell Publishing
Referencias:
Año: 2005 vol. 21 p. 311 - 317
ISSN:
0905-4383
Resumen:
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/cm2) 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 (O2_ _) 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 O2_ _ 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.