Ultraviolet Radiation Increases the Toxicity of Pyrene, 1-Aminopyrene and 1-Hydroxypyrene to Human Keratinocytes

Ekunwe, Stephen I.N.; Hunter, Rochelle D; Hwang, Huey‐Min

doi:10.3390/ijerph2005010058

Cited by 14 publications

(10 citation statements)

References 14 publications

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“…The relative photocytotoxicity is: 1-HP ~ 1-AP ~ Pyrene > 1-BP > 1-NP. These results are similar to the previously reported in both HaCaT and Jurkat cells using some of the similar compounds 2,36,37 .…”

Section: Discussionsupporting

confidence: 92%

“…We attribute this difference to the better solubility in cell media for 1-AP and 1-HP, which each possess a polar group, and to their stronger interaction with cellular DNA. For example, 1-HP binds strongly to calf thymus DNA 18 ; 1-AP and 1-HP can strongly cause DNA single strand cleavage in plasmid DNA 18,19 ; and a [ 3 H]-thymidine incorporation test showed that 1-AP and 1-HP were more toxic to keratinocyte cells than pyrene 37 .…”

Section: Discussionmentioning

confidence: 99%

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DNA damage and repair of human skin keratinocytes concurrently exposed to pyrene derivatives and UVA light

Fullove

2013

Toxicol. Res.

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Polycyclic aromatic hydrocarbons (PAHs), a class of mutagenic environmental contaminants, insert toxicity through both metabolic activation and light irradiation. Pyrene, one of the most widely studied PAHs, along with its mono-substituted derivatives, 1-amino, 1-bromo, 1-hydroxy, and 1-nitropyrene, were chosen to study the effect of substituents on their phototoxicity, DNA damage and repair. Both alkaline Comet assay, which detects direct DNA damages, and Fpg endonuclease Comet assay, which detects oxidative DNA damages, were conducted at 0, 2, 4, 8, and 24 h of incubation of the cells in minimal growth medium after concomitant exposure to pyrene derivatives and UVA light. All these compounds are photocytotoxic and the phototoxicity is both incubation time and PAH dose dependent; whereas, those without light are not toxic. The LC50 obtained are in the range of 3.5 – 9.3 µM. Cellular DNA damages, both direct and oxidative, are observed immediately after the cells are treated with UVA light and the pyrene derivatives at a concentration of 1.0 µM. The amount of DNA damages (both direct and oxidative) increase from 0 to 4 h of incubation. After 4 hours, subsequent damage induction declines, and this is perceived to be mainly through DNA repair. After longer incubation of 8 h, the damaged cellular DNA start to be repaired, resulting in greatly reduced amount of DNA damages, and the DNA damage reaches the minimum at 24 h of incubation. 1-Amopyrene and 1-hydroxypyrene cause more DNA oxidative damages immediately after the exposure (0 h of incubation), and these damages are repaired within the same timeframe as the other tested compounds. The oxidative DNA damages caused by 1-bromopyrene are repaired starting at 2 h of incubation, earlier than the damages caused by all the other compounds.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

DNA damage and repair of human skin keratinocytes concurrently exposed to pyrene derivatives and UVA light

Fullove

2013

Toxicol. Res.

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“…UVR is known to increase the toxicity of PAHs through photoactivation and photomodification [39]. Skin damage caused by exposure to BaP is further increased by exposure to both UV-A and UV-B radiation.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Damage to Nucleic Acids and Benzo(a)pyrene-7,8-diol-9,10-epoxide-DNA Adducts and Chromosomal Aberration in Children with Psoriasis Repeatedly Exposed to Crude Coal Tar Ointment and UV Radiation

Borská

Andrýs

Krejsek

et al. 2014

Oxidative Medicine and Cellular Longevity

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The paper presents a prospective cohort study. Observed group was formed of children with plaque psoriasis (n=19) treated by Goeckerman therapy (GT). The study describes adverse (side) effects associated with application of GT (combined exposure of 3% crude coal tar ointment and UV radiation). After GT we found significantly increased markers of oxidative stress (8-hydroxy-2′-deoxyguanosine, 8-hydroxyguanosine, and 8-hydroxyguanine), significantly increased levels of benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE) DNA adducts (BPDE-DNA), and significantly increased levels of total number of chromosomal aberrations in peripheral lymphocytes. We found significant relationship between (1) time of UV exposure and total number of aberrated cells and (2) daily topical application of 3% crude coal tar ointment (% of body surface) and level of BPDE-DNA adducts. The findings indicated increased hazard of oxidative stress and genotoxic effects related to the treatment. However, it must be noted that the oxidized guanine species and BPDE-DNA adducts also reflect individual variations in metabolic enzyme activity (different extent of bioactivation of benzo[a]pyrene to BPDE) and overall efficiency of DNA/RNA repair system. The study confirmed good effectiveness of the GT (significantly decreased PASI score).

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“…Cells were seeded on 96-well plates (20,000 cells/well), grown in DMEM with 10% FBS, and starved overnight in the absence of serum prior to treatments [24]. Cells were then exposed to HMGb1 at various concentrations for 24 h. After removing the medium, a 0.05% solution of neutral red was added to each well, followed by incubation for 3 h at 37°C.…”

Section: Neutral Red Uptake (Nru) and Crystal Violet (Cv) Assaysmentioning

confidence: 99%

Hmgb1 Promotes Wound Healing of 3T3 Mouse Fibroblasts via Rage-Dependent ERK1/2 Activation

Ranzato

Patrone

Pedrazzi

et al. 2010

Cell Biochem Biophys

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HMGb1 is a nuclear protein playing a role in DNA architecture and transcription. This protein has also been shown to function as a cytokine and to stimulate keratinocyte scratch wound healing. Due to the importance of finding new wound healing molecules, we have studied the effects of HMGb1 on fibroblasts, another major skin cell type, using the NIH 3T3 line. HMGb1 expression in these cells was assessed by Western blot, while its nuclear localization was pointed out by confocal immunofluorescence. HMGb1-induced cell proliferation with a maximum at a concentration of 10 nM, and such a dose also stimulated cell migration and scratch wound healing. Western blot analysis showed that HMGb1 activates ERK1/2, while the use of an anti-RAGE receptor-blocking antibody and of the selective MEK1/2 inhibitor PD98059 blocked ERK1/2 activation and wound healing responses to HMGb1. Taken together data show that HMGb1 promotes 3T3 fibroblast wound healing by inducing cell proliferation and migration, and that this occurs through the activation of the RAGE/MEK/ERK pathway. In conclusion, HMGb1 seems a good candidate for the development of medical treatments to be used on chronic or severe wounds.

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Ultraviolet Radiation Increases the Toxicity of Pyrene, 1-Aminopyrene and 1-Hydroxypyrene to Human Keratinocytes

Cited by 14 publications

References 14 publications

DNA damage and repair of human skin keratinocytes concurrently exposed to pyrene derivatives and UVA light

DNA damage and repair of human skin keratinocytes concurrently exposed to pyrene derivatives and UVA light

Oxidative Damage to Nucleic Acids and Benzo(a)pyrene-7,8-diol-9,10-epoxide-DNA Adducts and Chromosomal Aberration in Children with Psoriasis Repeatedly Exposed to Crude Coal Tar Ointment and UV Radiation

Hmgb1 Promotes Wound Healing of 3T3 Mouse Fibroblasts via Rage-Dependent ERK1/2 Activation

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