Next Article in Journal
Expression and Functional Studies on the Noncoding RNA, PRINS
Next Article in Special Issue
Quantitative Profiling of DNA Damage and Apoptotic Pathways in UV Damaged Cells Using PTMScan Direct
Previous Article in Journal
Changes in Translational Control after Pro-Apoptotic Stress
Previous Article in Special Issue
UVA Irradiation of Dysplastic Keratinocytes: Oxidative Damage versus Antioxidant Defense
Article Menu

Export Article

Open AccessReview
Int. J. Mol. Sci. 2013, 14(1), 191-204; doi:10.3390/ijms14010191

The Role of Photolabile Dermal Nitric Oxide Derivates in Ultraviolet Radiation (UVR)-Induced Cell Death

1
Department of Plastic and Reconstructive Surgery, Hand Surgery, and Burn Center, Medical Faculty, RWTH Aachen University, Pauwelsstr. 30, D-52074 Aachen, Germany
2
Department of Trauma and Hand Surgery, Medical Faculty of the Heinrich-Heine-University, 40225 Düsseldorf, Germany
*
Author to whom correspondence should be addressed.
Received: 26 October 2012 / Revised: 11 December 2012 / Accepted: 12 December 2012 / Published: 21 December 2012
(This article belongs to the Special Issue UV-Induced Cell Death 2012)
View Full-Text   |   Download PDF [324 KB, uploaded 19 June 2014]   |  

Abstract

Human skin is exposed to solar ultraviolet radiation comprising UVB (280–315 nm) and UVA (315–400 nm) on a daily basis. Within the last two decades, the molecular and cellular response to UVA/UVB and the possible effects on human health have been investigated extensively. It is generally accepted that the mutagenic and carcinogenic properties of UVB is due to the direct interaction with DNA. On the other hand, by interaction with non-DNA chromophores as endogenous photosensitizers, UVA induces formation of reactive oxygen species (ROS), which play a pivotal role as mediators of UVA-induced injuries in human skin. This review gives a short overview about relevant findings concerning the molecular mechanisms underlying UVA/UVB-induced cell death. Furthermore, we will highlight the potential role of cutaneous antioxidants and photolabile nitric oxide derivates (NODs) in skin physiology. UVA-induced decomposition of the NODs, like nitrite, leads not only to non-enzymatic formation of nitric oxide (NO), but also to toxic reactive nitrogen species (RNS), like peroxynitrite. Whereas under antioxidative conditions the generation of protective amounts of NO is favored, under oxidative conditions, less injurious reactive nitrogen species are generated, which may enhance UVA-induced cell death.
Keywords: UVA; nitrite; nitric oxide; cell death; lipid peroxidation; apoptosis; necrosis; antioxidants UVA; nitrite; nitric oxide; cell death; lipid peroxidation; apoptosis; necrosis; antioxidants
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Opländer, C.; Suschek, C.V. The Role of Photolabile Dermal Nitric Oxide Derivates in Ultraviolet Radiation (UVR)-Induced Cell Death. Int. J. Mol. Sci. 2013, 14, 191-204.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top