The effects of the melatonin on ultraviolet-B irradiated cultured dermal fibroblasts

Ryoo, Young Wook; Suh, Seong Il; Mun, Kyo‐Cheol; Kim, Byung Chun; Lee, Kyu Suk

doi:10.1016/s0923-1811(01)00133-5

Cited by 71 publications

(65 citation statements)

References 21 publications

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“…Because of its antioxidant activity, melatonin was tested as to its ability to influence apoptosis induced by X-irradiation in skin fibroblasts. In this system, melatonin prevented cell death caused by irradiation and decreased lipid peroxidation without affecting p21 or p53 genes, which are related to X-ray-induced apoptosis [171]. In addition, melatonin was shown to diminish apoptotic cell death induced by ultraviolet-B radiation of dermal fibroblasts at very low concentrations (1 nM or 100 nM).…”

Section: Melatonin and Apoptosis In Peripheral Tissuesmentioning

confidence: 87%

Melatonin and cell death: differential actions on apoptosis in normal and cancer cells

Sainz

Mayo

Rodríguez

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

275

218

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Melatonin is a natural compound synthesized by a variety of organs. It has been shown to function as a cell-protective agent. Since 1994, when the first paper was published documenting the role of melatonin in apoptosis, the number of reports in this area has increased rapidly. Much of the research conducted falls into three major categories: first, the role of melatonin in inhibiting apoptosis in immune cells; second, the role of melatonin in preventing neuronal apoptosis and finally, the role of melatonin in increasing apoptotic cell death in cancer cells. The mechanisms whereby melatonin influences apoptosis have not clarified, although a number of mechanistic options have been suggested. Apoptotic cell death is a physiological phenomenon related to homeostasis and proper functioning of tissues and organs; however, a failure in the apoptotic program is related to a number of diseases. The participation of melatonin in apoptosis in numerous cell types and its potential importance in a variety of diseases such as immunodeficiency, neurodegeneration and cancer is summarized in this review.

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Section: Melatonin and Apoptosis In Peripheral Tissuesmentioning

confidence: 87%

Melatonin and cell death: differential actions on apoptosis in normal and cancer cells

Sainz

Mayo

Rodríguez

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

275

218

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“…On the basis of these data we concluded that melatonin, its precursor NAS, and its metabolites 6-hydroxymelatonin, AFMK, 5-MT, all of which are endogenously produced in keratinocytes, protect these cells against UVB-induced oxidative stress and DNA damage [141]. It was also noted that for UV-exposed fibroblasts, only 56% of the cells survived upon UV exposure (140 mJ/cm 2 ), while cells pre-incubated with 10−9 M melatonin caused a cell survival rate of 92.5% which was paralleled by significant reduction of lipid peroxidation and cell death [146]. In addition, comparative experiments using UV-treated fibroblasts showed a similar correlation in cell viability in presence of 10−7 M melatonin [147].…”

Section: Melatonin As a “Guardian” Of The Genome And Cellular And mentioning

confidence: 99%

Local Melatoninergic System as the Protector of Skin Integrity

Słomiński

Kleszczyński

Semak

et al. 2014

IJMS

132

169

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The human skin is not only a target for the protective actions of melatonin, but also a site of melatonin synthesis and metabolism, suggesting an important role for a local melatoninergic system in protection against ultraviolet radiation (UVR) induced damages. While melatonin exerts many effects on cell physiology and tissue homeostasis via membrane bound melatonin receptors, the strong protective effects of melatonin against the UVR-induced skin damage including DNA repair/protection seen at its high (pharmocological) concentrations indicate that these are mainly mediated through receptor-independent mechanisms or perhaps through activation of putative melatonin nuclear receptors. The destructive effects of the UVR are significantly counteracted or modulated by melatonin in the context of a complex intracutaneous melatoninergic anti-oxidative system with UVR-enhanced or UVR-independent melatonin metabolites. Therefore, endogenous intracutaneous melatonin production, together with topically-applied exogenous melatonin or metabolites would be expected to represent one of the most potent anti-oxidative defense systems against the UV-induced damage to the skin. In summary, we propose that melatonin can be exploited therapeutically as a protective agent or as a survival factor with anti-genotoxic properties or as a “guardian” of the genome and cellular integrity with clinical applications in UVR-induced pathology that includes carcinogenesis and skin aging.

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“…Furthermore, the fundamental role of melatonin in the protection of the cell from external and internal stresses, including high-energy ultraviolet wavelengths of solar radiation, and in maintenance of cellular homeostasis has been extensively studied over the last decade (Yu and Reiter, 1993; Reiter, 1996; Karbownik et al, 2001; Tan et al, 2003; Leon et al, 2004; Rodriguez et al, 2004). A protective effect of melatonin against UV radiation has already been documented in human keratinocytes, dermal fibroblasts, leukocytes and in the rat lens (Bardak et al, 2000; Nickel and Wohlrab, 2000; Fischer et al, 2001, 2002, 2004; Kim et al, 2001; Ryoo et al, 2001; Lee et al, 2003). …”

Section: Introductionmentioning

confidence: 96%

The melatonin-producing system is fully functional in retinal pigment epithelium (ARPE-19)

Żmijewski

Sweatman

Slominski

2009

Molecular and Cellular Endocrinology

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Since melatonin production has been documented in extrapineal and extraneuronal tissues, we investigated the expression of molecular elements of the melatoninergic system in human RPE cells (ARPE-19). The expression of key enzymes for melatonin synthesis: tryptophan hydroxylases (TPH1 and TPH2); arylalkylamine N-acetyltransferase (AANAT) and hydroxyindole-O-methyltransferase (HIOMT)was detected in ARPE-19 cells using RT-PCR.TPH1 and AANAT proteins were detected in ARPE by Western blotting, while sequential metabolism of tryptophan, serotonin and N-acetylserotonin to melatonin was shown by RPHPLC. We also demonstrated, by means of RT-PCR, that ARPE expressed mRNA encoding the melatonin receptors: MT2 (but not MT1), two isoforms of nuclear receptor (RORα1 and RORα4/RZR1), and quinone oxidoreductase (NQO2). By analogy with other peripheral tissues, for example the skin, the expression of these metabolic elements in RPE cells suggests that the RPE represents an additional source of melatonin in the eye, to regulate local homeostasis and prevent from oxidative damage in intra-, auto- and/or paracrine fashions.

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The effects of the melatonin on ultraviolet-B irradiated cultured dermal fibroblasts

Cited by 71 publications

References 21 publications

Melatonin and cell death: differential actions on apoptosis in normal and cancer cells

Melatonin and cell death: differential actions on apoptosis in normal and cancer cells

Local Melatoninergic System as the Protector of Skin Integrity

The melatonin-producing system is fully functional in retinal pigment epithelium (ARPE-19)

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