Sensitization of skin fibroblasts to UVA by excess iron

Morlière, Patrice; Salmon, S.; Aubailly, M.; Risler, Arnaud; Santús, René

doi:10.1016/s0304-4165(96)00106-7

Cited by 40 publications

(22 citation statements)

References 25 publications

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“…Several lines of evidence strengthen this model. Firstly, UVA-mediated membrane damage in human skin fibroblasts could be prevented in cells pre-treated with iron chelators, and conversely could be enhanced in ironloaded cells (Morliere et al, 1991(Morliere et al, , 1997Punnonen et al, 1991;. Secondly, UVA-mediated activation of NF-kB appeared to be correlated with membrane damage, since it could be prevented by the membrane antioxidants BHT and a-tocopherol acetate as previously demonstrated by and as shown in Fig 6, this study.…”

Section: Figuresupporting

confidence: 80%

Ultraviolet A Radiation-Induced Immediate Iron Release Is a Key Modulator of the Activation of NF-κB in Human Skin Fibroblasts

Reelfs

Tyrrell

Pourzand

2004

Journal of Investigative Dermatology

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Ultraviolet A (UVA, 320-400 nm) radiation, an oxidizing component of sunlight, leads to an immediate increase in the labile iron in human skin fibroblasts. Exposure of skin fibroblasts to UVA radiation is also known to induce nuclear factor-kappaB (NF-kappaB) DNA-binding activity, although the underlying mechanism is unclear. We report here that in skin fibroblasts, the extent of NF-kappaB activation by UVA tightly correlates with the level of "UVA-induced" labile iron release as shown by both iron chelation and iron loading treatments. Furthermore, our data indicate that the slow kinetics of induction of NF-kappaB by UVA relative to other oxidants previously studied is due to a transient increase in permeability of nuclear membrane to proteins and occurs as a result of labile iron-mediated damage to nuclear membrane. Since in addition to iron chelators, lipid peroxidation inhibitors also decrease the UVA-mediated induction of NF-kappaB, we propose that the rapid release of labile iron by UVA might act as a catalyst to exacerbate the generation of lipid secondary messengers in skin cell membranes that are responsible for induction of NF-kappaB. This novel role for iron in amplifying NF-kappaB mobilization in response to UVA-induced oxidative stress aids understanding of its involvement in UV-induced skin inflammation.

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Section: Figuresupporting

confidence: 80%

Ultraviolet A Radiation-Induced Immediate Iron Release Is a Key Modulator of the Activation of NF-κB in Human Skin Fibroblasts

Reelfs

Tyrrell

Pourzand

2004

Journal of Investigative Dermatology

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“…4). In contrast, vitamin E not only inhibits lipid peroxidation in UVAexposed fibroblasts [9], but also impedes membrane injury [9,10,30] and can partly restore cell viability after UVA irradiation. Indeed, the exposure of cultured human skin fibroblasts from four different donors to 60 J/cm 2 dropped the colony-forming ability to 5.0Ϯ 0.9, 9.6Ϯ 4.3, 7.3 Ϯ 1.3 and 19.4Ϯ 4.9% of the control, respectively (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…The neutral red uptake assay was performed according to the method of Lasarow [29] and as earlier detailed [30]. Absorbances measured at 550 nm in a 96-well microplate reader, are the mean ϮSD of triplicates and are normalized to the absorbance of untreated sham-irradiated cells taken as 100.…”

Section: Methodsmentioning

confidence: 99%

Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Morlière

Santús

1998

European Journal of Biochemistry

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Exposure of cultured normal human skin fibroblasts to ultraviolet A triggers lipid peroxidation. In sharp contrast with the tert-butylhydroperoxide-induced lipid peroxidation, the ultraviolet-A-induced lipid peroxidation is inhibited by treating cells with diethyldithiocarbamate. Diethyldithiocarbamate decreases superoxide dismutase activity and, to a lesser extent, the total glutathione level. Catalase and glutathione peroxidase, however, are unaffected. The decrease in the superoxide dismutase activity parallels an inhibition of H 2 O 2 formation in both irradiated and unirradiated cells. The protection against lipid peroxidation may thus be associated with superoxide dismutase inhibition. Membrane damage revealed by neutral red uptake is not prevented by diethyldithiocarbamate.

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“…These low-molecular-mass complexes can initiate free radical damage as they supply iron ions in a form capable of accelerating free radical reactions and lipid peroxidation (25). In this regard, iron sensitizes cultured human skin fibroblasts to the ultraviolet A (UVA) radiation when cells are treated with low molecular mass complexes or exposed to high ferritin and holotransferrin concentrations with evidence of increased membrane lipid peroxidation and cytotoxicity (26) and activation of MAP kinases (27). The present study, showing that the extracellular space is the major site of excess iron deposition in the skin of patients with HH (Figs IB and 2), might provide evidence about the lack of notable UVA-induced skin sensitization.…”

Section: Discussionmentioning

confidence: 99%

Distribution and Quantitation of Skin Iron in Primary Haemochromatosis: Correlation with Total Body Iron Stores in Patients Undergoing Phlebotomy

Pinheiro¹,

Silva²,

Fleming³

et al. 2014

Acta Derm Venerol

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Measurement of the concentration of iron in the skin, if correlated with total body iron stores, may enable better informed decisions on when to initiate, change or stop therapy in hereditary heamochromatosis. Naïve haemochromatosis patients with iron overload and with C282Y and/or H63D HFE mutations were evaluated at the following time-points: disease diagnosis, end of the therapy programme, and 6 months after the end of therapy. The distribution and concentration of iron in the skin were assessed by quantitative nuclear microscopy methods, in parallel with serum and plasma iron concentration. Iron content in the liver was determined by nuclear magnetic resonance. Iron accumulated in the epidermis; its concentration increased from outer to inner layers, being maximal in the basal layer (7.33 ± 0.98 µmol/g). At all 3 time-points, most of the iron was associated with the extracellular space. During the phlebotomy programme the iron content of the skin and the liver decreased by a factor of 2. These data suggest that measurements of iron concentration in the epidermis, which is a readily accessible tissue, reflect iron overload in the liver.

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Sensitization of skin fibroblasts to UVA by excess iron

Cited by 40 publications

References 25 publications

Ultraviolet A Radiation-Induced Immediate Iron Release Is a Key Modulator of the Activation of NF-κB in Human Skin Fibroblasts

Ultraviolet A Radiation-Induced Immediate Iron Release Is a Key Modulator of the Activation of NF-κB in Human Skin Fibroblasts

Pro‐oxidant role of superoxide dismutase in ultraviolet‐A‐induced lipid peroxidation in cultured normal human skin fibroblasts

Distribution and Quantitation of Skin Iron in Primary Haemochromatosis: Correlation with Total Body Iron Stores in Patients Undergoing Phlebotomy

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