Journal of Investigative Dermatology

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Triplet-Energy Quenching Functions of Antioxidant Molecules

Antioxidants-Basel

Cloned Mouse Melanocyte Lines Carrying the Germline Mutations Albino and Brown - Complementation in Culture

Development

A line of non-tumorigenic mouse melanocytes, syngeneic with the B16 melanoma and requiring a tumour promoter for growth

Int J Cancer

UV Signature Mutations

Photochem Photobiol

Formation of UV-induced DNA damage contributing to skin cancer development

Photochem Photobiol Sci

Topical drug rescue strategy and skin protection based on the role of Mc1r in UV-induced tanning

Nature

Sunburns and risk of cutaneous melanoma: Does age matter? A comprehensive meta-analysis

Ann Epidemiol

Biological selectivity and functional aspects of protein tyrosine nitration

Biochem Biophys Res Commun

Roles of UVA radiation and DNA damage responses in melanoma pathogenesis

Environ Mol Mutagen

Wavelength dependence of oxidative DNA damage induced by UV and visible light

Carcinogenesis

Antigen structural requirements for recognition by a cyclobutane thymine dimer-specific monoclonal antibody

Nucleic Acids Res

The eumelanin intermediate 5,6-dihydroxyindole-2-carboxylic acid is a messenger in the cross-talk among epidermal cells

J Invest Dermatol

8-Oxoguanine formation induced by chronic UVB exposure makes Ogg1 knockout mice susceptible to skin carcinogenesis

Cancer Res

Murine cutaneous mastocytosis and epidermal melanocytosis induced by keratinocyte expression of transgenic stem cell factor

J Exp Med

Biochemistry of melanin synthesis: in vivo effects of MSH on tyrosinase and melanogenesis of pigmentary system

Yale J Biol Med

Lifetime Sunburn Trajectories and Associated Risks of Cutaneous Melanoma and Squamous Cell Carcinoma Among a Cohort of Norwegian Women

Jama Dermatol

Prevalence of UV Mutational Signatures Among Cutaneous Primary Tumors

JAMA Netw Open

An ultraviolet-radiation-independent pathway to melanoma carcinogenesis in the red hair/fair skin background

Cyclobutane pyrimidine dimers are predominant DNA lesions in whole human skin exposed to UVA radiation

Proc Natl Acad Sci U S A

UVA-induced cyclobutane pyrimidine dimers in DNA: a direct photochemical mechanism?

Org Biomol Chem

Nucleotide excision repair deficiency in melanoma in response to UVA

Exp Hematol Oncol

Synthesis and characterization of melanins from dihydroxyindole-2-carboxylic acid and dihydroxyindole

Pigment Cell Res

Nitric oxide and peroxynitrite in health and disease

Physiol Rev

UV wavelength-dependent DNA damage and human non-melanoma and melanoma skin cancer

Photoch Photobio Sci

Unanticipated role of melanin in causing carcinogenic cyclobutane pyrimidine dimmers

Mol Cell Oncol

Photochemistry. Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure

Science

Identification of potentially cytotoxic lesions induced by UVA photoactivation of DNA 4-thiothymidine in human cells

Time kinetics of cyclobutane pyrimidine dimer formation by narrowband and broadband UVB irradiation

J Dermatol Sci

The inherent cytotoxicity of melanin precursors: a revision

Biochim Biophys Acta

Stem cell factor rescues tyrosinase expression and pigmentation in discreet anatomic locations in albino mice

Pigment Cell Melanoma Res

Significance of melanin distribution in the epidermis for the protective effect against UV light

Sci Rep

Prolonged DNA damage at suberythemal UV dose - Dependency on skin type and age

J Photochem Photobiol B

Cyclobutane pyrimidine dimers (CPDs) are the major form of DNA damage induced by ultraviolet (UV) radiation. While CPDs form instantaneously during UV exposure, our prior studies demonstrated that melanin chemiexcitation, in which UV-induced peroxynitrite oxidizes melanin into excited-state intermediates, continues to generate CPDs for hours after UV exposure ends. These "delayed" CPDs (dCPDs) contribute up to 50% of the total CPD burden. Although melanin's involvement is well established, it remains unclear whether active melanin biosynthesis is required, or if the mere presence of pigment is sufficient. To address this, we developed a de-pigmentation-re-pigmentation system using cultured melanocytes. Cells were de-pigmented in tyrosine-deficient medium and re-pigmented either by reintroducing tyrosine or by supplementing with 5,6-dihydroxyindole-2-carboxylic acid (DHICA), a melanin monomer that polymerizes non-enzymatically. In both conditions, dCPD formation was restored. Notably, DHICA treatment alone was sufficient to induce pigmentation and dCPD formation even in tyrosinase-deficient isogenic albino melanocytes. Pigment accumulation was also associated with nitric oxide synthase (NOS) activity, a key contributor to chemiexcitation, although the mechanisms linking melanin-synthesis to NOS activity remain to be elucidated. These findings demonstrated that pigment presence, not biosynthesis, as the key determinant of dCPD formation, with broad implications for photobiology, pigmentation, and skin cancer risk.

Melanin-Driven Delayed CPD Formation Is Independent of Melanin Biosynthesis Pathway.

Melanin-Driven Delayed CPD Formation Is Independent of Melanin Biosynthesis Pathway

Melanin-Driven Delayed CPD Formation Is Independent of Melanin Biosynthesis Pathway

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