Abstract
Long-wavelength ultraviolet radiation (UVA) can cause cancer. A carcinogenic mechanism involved may be the induction of harmful reactive oxygen species resulting from photodynamic effects. UVA is generally assumed to induce photodynamic effects, but evidence from experiments with viable biological materials has been indirect until present. Here we measured the induction of (lipid) hydroperoxides as direct indicators of photodynamic reactions. Cultured human fibroblasts were irradiated with 10 J UVA/cm2. The induced hydroperoxides were measured by an enzymatic method using glutathione peroxidase and glutathione reductase (GR). Additionally, reduced glutathione (GSH) was determined as parameter for the constitutive antioxidant defense. UVA was found to increase lipid hydroperoxides in fibroblasts by 116% (p< 0.001), when compared to nonirradiated controls. Conversely GSH was decreased in the irradiated cells by 51% (p< 0.001). Because of the induced hydroperoxides, it is concluded that the UVA effects were mediated by a photodynamic mechanism. The photodynamic mechanism resulted in the formation of reactive oxygen species and the consumption of constitutive antioxidants. This suggests a role for antioxidants during the photodynamic mechanism. Photodynamic mechanisms may play a crucial role in carcinogenic events, especially after UVA.
Keywords
- Glutathione Reductase
- Lipid Hydroperoxide
- Arachidonic Acid Release
- Photodynamic Action
- Linoleate Hydroperoxide
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1995 Springer-Verlag Berlin · Heidelberg
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Schmitz, S. et al. (1995). Photodynamic Action of Ultraviolet A: Induction of Cellular Hydroperoxides. In: Garbe, C., Schmitz, S., Orfanos, C.E. (eds) Skin Cancer: Basic Science, Clinical Research and Treatment. Recent Results in Cancer Research, vol 139. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78771-3_4
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DOI: https://doi.org/10.1007/978-3-642-78771-3_4
Publisher Name: Springer, Berlin, Heidelberg
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