Nonenzymatic Nitric Oxide Formation during UVA Irradiation of Human Skin: Experimental Setups and Ways to Measure

Suschek, Christoph V.; Paunel, Adnana N.; Kolb-Bachofen, Victoria

doi:10.1016/s0076-6879(05)96048-5

Cited by 21 publications

(10 citation statements)

References 23 publications

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“…The concentrations of nitrite and nitrosated compounds (RXNO) were quantified by iodine/iodide-based assay NO-analyzer CLD 88 (Ecophysics) as described elsewhere [40,41]. To determine total nitrite, nitrate and RXNO concentrations, collectively termed nitric oxide derivates (NOD), samples were added to 0.1 mol/l vanadium (III) chloride in 1 M hydrochloric acid refluxing at 95°C under nitrogen [42].…”

Section: Detection Of Nitrite Nitrate and Rxnomentioning

confidence: 99%

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The topical use of non-thermal dielectric barrier discharge (DBD): Nitric oxide related effects on human skin

et al. 2015

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Section: Detection Of Nitrite Nitrate and Rxnomentioning

confidence: 99%

“…After plasma application human skin specimens were homogenized as described elsewhere [41]. For quantification of nitrite/ nitrite/RXNO a volume of 100 μl was injected directly into the respective reactions solutions as described above.…”

Section: Quantification Of Nitrite/nitrate/rxno In Skin Tissuementioning

confidence: 99%

The topical use of non-thermal dielectric barrier discharge (DBD): Nitric oxide related effects on human skin

et al. 2015

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“…Regarding UVA-induced cell membrane damage, it had been shown that the radical nitric oxide can inhibit lipid peroxidation by scavenging lipid peroxyl radicals and/or inhibiting initiators of lipid peroxidation, respectively, and, consequently, also inhibits UVA-induced cell death via apoptosis or necrosis [36–40]. However, NO may react with superoxide to peroxynitrite, which initiates lipid peroxidation itself and oxidizes lipid soluble antioxidants [41].…”

Section: Uvr-induced Cell Damagementioning

confidence: 99%

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

Opländer

Suschek

2012

IJMS

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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.

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“…The concentrations of nitrite were quantified by an iodine/iodide-based assay using a NO-analyzer (CLD 88, Ecophysics, Munich, Germany) as described elsewhere. 38,39 To determine total nitrite and nitrate concentration, samples were added to 0.1 M vanadium (III) chloride in 1 M hydrochloric acid refluxing at 95°C under nitrogen. 39…”

Section: G Detection Of Nitrite and Nitratementioning

confidence: 99%

Acidification and Nitrite/Nitrate Accumulation by Nonthermal Dielectric Barrier Discharge (DBD) Affect Human Dermal Fibroblasts

et al. 2015

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Reactive species generated by dielectric barrier discharge (DBD) may exert many biological effects including cell toxicity. The reactive nitrogen species nitrogen dioxide hydrolyses in water resulting in acidification and increased osmolality by the formation of nitric acid and nitrous acid. Regarding the small media volumes in which cells were maintained in vitro during plasma treatment, here we address the question of whether cell toxicity effects of plasma may also be mediated by changes of pH, osmolality, and nitrite/nitrate concentrations. DBD treatment led to a treatment time-dependent increase of osmolality, acidification, and accumulation of nitrite and nitrate in buffer and cell culture media. In small buffer volumes, DBD treatment rapidly broke down the buffer capacity, and pH fell below the physiological range. The obtained nitrite/nitrate concentrations were considerably higher than those found in blood and tissues. DBD-treated buffer and acidified buffer containing nitrite/nitrate reduced cell viability of human dermal fibroblasts in the same magnitude. The antioxidant sodium ascorbate could not reverse this effect, whereas it protected fibroblasts partially during DBD treatments. Our results indicate that apart from reactive species, DBD-induced chemical and physical changes in the environment of cells may be responsible for many observed biological effects.

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Nonenzymatic Nitric Oxide Formation during UVA Irradiation of Human Skin: Experimental Setups and Ways to Measure

Cited by 21 publications

References 23 publications

The topical use of non-thermal dielectric barrier discharge (DBD): Nitric oxide related effects on human skin

The topical use of non-thermal dielectric barrier discharge (DBD): Nitric oxide related effects on human skin

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

Acidification and Nitrite/Nitrate Accumulation by Nonthermal Dielectric Barrier Discharge (DBD) Affect Human Dermal Fibroblasts

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