Singlet oxygen is an early intermediate in cytokine‐dependent ultraviolet‐A induction of interstitial collagenase in human dermal fibroblasts in vitro

Wlaschek, Meinhard; Wenk, Jutta; Brenneisen, Peter; Briviba, Karlis; Schwarz, Agatha; Sies, Helmut; Scharffetter‐­Kochanek, Karin

doi:10.1016/s0014-5793(97)00919-8

Cited by 126 publications

(88 citation statements)

References 34 publications

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“…To determine the possibility of type II reactions, we analysed the effect of enhancers and quenchers of singlet oxygen on ROS production after light-activated Photolon TM treatment. D 2 O, has been reported to significantly prolong the lifetime of singlet oxygen and hence serves as an enhancer (Wlaschek et al, 1997). If activated Photolon TM produced singlet oxygen species; we anticipated that ROS production would be enhanced with D 2 O.…”

Section: Photolon Tm -Induced Cell Death Occurs Via Type I Ros Reactionsmentioning

confidence: 98%

Photolon™, a chlorin e6 derivative, triggers ROS production and light-dependent cell death via necrosis

Copley

Watt

Wirtz

et al. 2008

The International Journal of Biochemistry & Cell Biology

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PhotolonTM is a photosensitiser with demonstrated potential as an anti-tumour agent. In this study, an in vitro investigation was performed to determine the mechanism of Photolon TM -induced cell death. Cell killing was observed in a light-dependent manner and light-activated Photolon TM resulted in a significant production of reactive oxygen species (ROS), which could be blocked by type I ROS scavengers. Inhibition of ROS production using Trolox prevented Photolon TM -induced cell death. Lightactivated Photolon TM caused no increase in caspase-3/7 activity, but a rapid increase in lactate dehydrogenase (LDH) release suggesting a loss of membrane integrity and subsequent cell death by necrosis. We conclude that the mechanism of Photolon TMinduced cell death involves the induction of ROS via a type I mechanism, which is ultimately responsible for cell killing by necrosis.

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Section: Photolon Tm -Induced Cell Death Occurs Via Type I Ros Reactionsmentioning

confidence: 98%

Photolon™, a chlorin e6 derivative, triggers ROS production and light-dependent cell death via necrosis

Copley

Watt

Wirtz

et al. 2008

The International Journal of Biochemistry & Cell Biology

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“…Recent reports of the UV-A irradiation of fibroblasts indicate that singlet oxygen is both an early intermediate in the signaling pathway of interstitial colleganase induction, preceding the synthesis of the proinflammatory cytokines interleukin 1 and interleukin 6 (43), and can activate JNKs (stress-activated kinases), which can affect gene expression (44). Correlation between UV-A and singlet oxygen also have been discussed for the induced synthesis of mRNA heme oxygenase-1 (45,46), colleganase (43,47,48), and intercellular adhesion molecule-1 (49). Whether t-UA is a major contributing source of the singlet oxygen that causes these responses requires more research.…”

Section: Biophysics: Hanson and Simonmentioning

confidence: 99%

Epidermaltrans-urocanic acid and the UV-A-induced photoaging of the skin

Hanson

Simon

1998

Proc. Natl. Acad. Sci. U.S.A.

146

115

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The premature photoaging of the skin is mediated by the sensitization of reactive oxygen species after absorption of ultraviolet radiation by endogenous chromophores. Yet identification of UV-A-absorbing chromophores in the skin that quantitatively account for the action spectra of the physiological responses of photoaging has remained elusive. This paper reports that the in vitro action spectrum for singlet oxygen generation after excitation of trans-urocanic acid mimics the in vivo UV-A action spectrum for the photosagging of mouse skin. The data presented provide evidence suggesting that the UV-A excitation of trans-urocanic acid initiates chemical processes that result in the photoaging of skin.Most of the visible signs of aging result from chronic exposure of the skin to ultraviolet radiation (1-2). Unlike chronologically aged skin that results from a general atrophy and a gradual decline in the production of the dermal matrix (3), UV-A (320-400 nm) photoaged skin is characterized by a gross increase in the elastic fibers (elastin, fibrillin, and desmosine) of the skin replacing the collagenated dermal matrix (elastosis) (4-5), an increase in glycosaminoglycans (4-5), collagen cross-linking, epidermal thickening (4-6), and an increase in the number of dermal cysts (7). The deep lines, leathered appearance, and the sagging of the skin surface typically associated with ''old age'' are thought to result from UV-induced photodamage to the skin and to occur over the course of a lifetime (3). Although obvious differences between photoaged and chronologically aged skin exist, the anatomic basis of the visible signs of photoaging is not understood fully (4, 8). Absorption of UV-A must induce photobiologic effects within the skin that lead to the visible and histological differences of photoaged skin, and, although the mechanisms by which UV-A-induced photodamage occur have not been completely determined, reactive oxygen species are postulated to play a role (9). The natural shift toward a more prooxidant state in chronologically aged skin then could be exacerbated by absorption of UV-A radiation by endogenous chromophores like NADH͞NADPH (10-14), tryptophan (15), and riboflavin (9), which then sensitize the formation of reactive oxygen species. Solar radiation has been shown both to reduce the antioxidant population in the skin (16) and to sensitize the production of reactive oxygen species such as singlet oxygen, hydrogen peroxide, and the superoxide anion (9-19), increasing the potential for reactions like the oxidation of lipids and proteins (17) that influence the degree of cross-linking between collagen and other proteins (9) within the skin.The first step toward identifying the chromophore(s) responsible for physiological changes, such as those seen in photoaged skin, is to match the action spectrum for the physiological change with the absorption spectrum of the chromophore (20). Once such a comparison is made, the pathways that lead to the physiological change can be unraveled. For example, the epid...

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“…UVA regulates the expression of various genes including heme oxygenase-1, matrix metalloproteinase-1, IL-1a/b, IL-6, intracellular adhesion molecule, STAT3, AP-1 and AP-2 (Basu- Modak and Tyrrell, 1993;Grether-Beck et al, 1996;Klotz et al, 1999;Maziere et al, 2001;Scharffetter-Kochanek et al, 1993;Wlaschek et al, 1997;Zhang et al, 2001b;Silvers and Bowden, 2002). Considerable work is currently underway to elucidate the signal transduction mechanisms that are induced by UVA.…”

Section: Introductionmentioning

confidence: 99%

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

2002

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Singlet oxygen is an early intermediate in cytokine‐dependent ultraviolet‐A induction of interstitial collagenase in human dermal fibroblasts in vitro

Cited by 126 publications

References 34 publications

Photolon™, a chlorin e6 derivative, triggers ROS production and light-dependent cell death via necrosis

Photolon™, a chlorin e6 derivative, triggers ROS production and light-dependent cell death via necrosis

Epidermaltrans-urocanic acid and the UV-A-induced photoaging of the skin

The role of p38 in UVA-induced cyclooxygenase-2 expression in the human keratinocyte cell line, HaCaT

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