Melanoma induction by ultraviolet A but not ultraviolet B radiation requires melanin pigment

Noonan, Frances P.; Zaidi, M. Raza; Wolnicka-Głubisz, Agnieszka; Anver, Miriam R.; Bahn, Jesse; Wielgus, Albert R.; Cadet, Jean; Douki, Thierry; Mouret, Stéphane; Tucker, Margaret A.; Popratiloff, Anastas; Merlino, Glenn; Fabo, Edward C. De

doi:10.1038/ncomms1893

Cited by 286 publications

(315 citation statements)

References 58 publications

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“…Concurrent with existing literature proposing 2 independent pathways to melanomagenesis corresponding to induction by UVA and UVB irradiation, respectively, the study found that albino mice on the same genetic background developed fewer tumors than their pigmented counterparts following UVA irradiation. There were no significant differences between the mouse model tumorigenesis following UVB exposure (34). In line with current understanding that aberrant melanin synthesis is indeed associated with an increase in oxidative stress (35), the authors proposed that the increase in melanomagenesis observed in black mice was a result of dysregulated melanin synthesis induced by UVA exposure.…”

Section: Discussionsupporting

confidence: 60%

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Boulton

Birch‐Machin

2014

FASEB j.

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Melanogenesis is a highly conserved process of cytophotoprotection from UV radiation present in many species. Although both mitochondrial function and UV radiation insults are well-documented promoters of increased cellular stress, their individual molecular relationships with skin pigmentation have not been clearly resolved. This study provides evidence for a direct relationship between cellular melanin content, superoxide flux, and mitochondrial function at complex II. Direct and significant correlation between increased pigmentation and complex II turnover was observed in genetically different melanoma cell lines of varied basal pigmentation states (P < 0.01). The same trend was also observed when comparing genetically identical cell cultures with increasing levels of induced pigmentation (P < 0.005). The observation of increased steady-state levels of the catalytic complex II succinate dehydrogenase subunit A alongside hyperpigmentation suggested coregulation of activity and pigment production (P < 0.01). The study also presents novel evidence for a relationship between hyperpigmentation and increased superoxide-generating capacity at complex II. By amperometrically monitoring superoxide flux from differently pigmented FM55 melanocytes and their isolated mitochondria, a dynamic and responsive relationship between pigmentation, complex II function, and intracellular superoxide generation was observed (P < 0.005). The data support hyperpigmentation as a protective antioxidant mechanism in response to complex II-mediated reactive oxygen species generation.-Boulton, S. J., Birch-Machin, M. A. Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II. FASEB J. 29, 346-353 (2015). www.fasebj.org

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Section: Discussionsupporting

confidence: 60%

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Boulton

Birch‐Machin

2014

FASEB j.

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“…Some reports claimed that UVA (320-380 nm) is the main cause of melanin synthesis and also melanoma appearance. This mechanism is related to reactions involving directly melanin, as the pigment absorbs the energy from the radiation and originates free radicals and other injurious species [158]. On the other hand, other reports indicate that UVB (280-320 nm) seems to initiate melanoma in a pigmentindependent manner, associated with a direct damaging action of that radiation on DNA [159].…”

Section: Melanin Functionsmentioning

confidence: 99%

Melanins: Skin Pigments and Much More—Types, Structural Models, Biological Functions, and Formation Routes

Solano

2014

New Journal of Science

441

431

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This review presents a general view of all types of melanin in all types of organisms. Melanin is frequently considered just an animal cutaneous pigment and is treated separately from similar fungal or bacterial pigments. Similarities concerning the phenol precursors and common patterns in the formation routes are discussed. All melanins are formed in a first enzymatically-controlled phase, generally a phenolase, and a second phase characterized by an uncontrolled polymerization of the oxidized intermediates. In that second phase, quinones derived from phenol oxidation play a crucial role. Concerning functions, all melanins show a common feature, a protective role, but they are not merely photoprotective pigments against UV sunlight. In pathogenic microorganisms, melanization becomes a virulence factor since melanin protects microbial cells from defense mechanisms in the infected host. In turn, some melanins are formed in tissues where sunlight radiation is not a potential threat. Then, their redox, metal chelating, or free radical scavenging properties are more important than light absorption capacity. These pigments sometimes behave as a doubleedged sword, and inhibition of melanogenesis is desirable in different cells. Melanin biochemistry is an active field of research from dermatological, biomedical, cosmetical, and microbiological points of view, as well as fruit technology.

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“…Another important parameter that may affect the distribution of UVA-mediated DNA degradation products is cell type. This was recently illustrated for melanocytes that are more susceptible than other cell types to UVA-induced oxidatively generated damage to DNA both as isolated cells (89,116) and in pigmented mice (117). A summary of the main information available on the distribution of DNA damage generated upon exposure of cells to UVB and UVA radiations is provided in Fig.…”

Section: Uva-mediated Oxidatively Generated Dna Damage In Cellsmentioning

confidence: 99%

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†

Cadet¹,

Mouret²,

Ravanat³

et al. 2012

Photochem & Photobiology

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270

251

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The survey focuses on recent aspects of photochemical reactions to cellular DNA that are implicated through the predominant formation of mostly bipyrimidine photoproducts in deleterious effects of human exposure to sunlight. Recent developments in analytical methods have allowed accurate and quantitative measurements of the main DNA photoproducts in cells and human skin. Highly mutagenic CC and CT bipyrimidine photoproducts, including cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) are generated in low yields with respect to TT and TC photoproducts. Another striking finding deals with the formation of Dewar valence isomers, the third class of bipyrimidine photoproducts that is accounted for by UVA-mediated isomerization of initially UVB generated 6-4PPs. Cyclobutadithymine (T< >T) has been unambiguously shown to be involved in the genotoxicity of UVA radiation. Thus, T< >T is formed in UVA-irradiated cellular DNA according to a direct excitation mechanism with a higher efficiency than oxidatively generated DNA damage that arises mostly through the Type II photosensitization mechanism. C<>C and C< >T are repaired at rates intermediate between those of T< >T and 6-4TT. Evidence has been also provided for the occurrence of photosensitized reactions mediated by exogenous agents that act either in an independent way or through photodynamic effects.

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Melanoma induction by ultraviolet A but not ultraviolet B radiation requires melanin pigment

Cited by 286 publications

References 58 publications

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Melanins: Skin Pigments and Much More—Types, Structural Models, Biological Functions, and Formation Routes

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†

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Melanoma induction by ultraviolet A but not ultraviolet B radiation requires melanin pigment

Cited by 286 publications

References 58 publications

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Impact of hyperpigmentation on superoxide flux and melanoma cell metabolism at mitochondrial complex II

Melanins: Skin Pigments and Much More—Types, Structural Models, Biological Functions, and Formation Routes

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions†

Contact Info

Product

Resources

About

Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions^†