UV-Induced Oxidative Stress and Photoaging

Wenk, Jutta; Brenneisen, Peter; Meewes, Christian; Wlaschek, Meinhard; Peters, Thorsten; Blaudschun, R.; Ma, W.; Kuhr, Lale; Schneider, Lars; Scharffetter‐­Kochanek, Karin

doi:10.1159/000060656

Cited by 194 publications

(150 citation statements)

References 49 publications

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“…There is convincing evidence that ROS are crucially involved in premature skin aging and in connective tissue destruction (Wenk et al, 2001). Therefore, it is suggested that the topical application of radical scavengers and antioxidants like vitamin E, vitamin C and their derivatives may prevent premature skin aging and indeed these substances are widely used (Dreher and Maibach, 2001).…”

Section: Mechanisms Of Uv-induced Apoptosis D Kulms Et Almentioning

confidence: 99%

DNA damage, death receptor activation and reactive oxygen species contribute to ultraviolet radiation-induced apoptosis in an essential and independent way

Kulms¹,

Zeise²,

Pöppelmann³

et al. 2002

Oncogene

231

160

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Section: Mechanisms Of Uv-induced Apoptosis D Kulms Et Almentioning

confidence: 99%

DNA damage, death receptor activation and reactive oxygen species contribute to ultraviolet radiation-induced apoptosis in an essential and independent way

Kulms¹,

Zeise²,

Pöppelmann³

et al. 2002

Oncogene

231

160

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“…24,25 Ultraviolet irradiation is known to be the source of oxidative stress due to the interaction of photons and intracellular chromophore, which can result in genetic damage and activation of redox reaction that can cause oxidative stress of cells. 26,27 To study the antioxidant activity of Moringa extract, we used an ethyl acetate fraction of the extract, which is rich in phenolic acid. Phenolic acid can interact with oxidative oxygen species, donate the hydroxyl ion to the reactive oxygen and lead to the less reactive oxygen form.…”

Section: Discussionmentioning

confidence: 99%

Moringa Oleifera Lam. Leaves Extract Reduces Human T-Cell Hyporesponsiveness and Dna Damage Induced by Oxidative Stress

Kooltheat¹,

Sranujit²,

Luetragoon³

et al. 2017

Int. J. Res. Ayurveda Pharm.

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Chronic inflammatory conditions lead to the generation of excessive reactive oxygen species which can give rise to T cell hyporesponsiveness. Thus there has been an interest to target these mediators with nutrients which have anti-oxidant properties. Accordingly Moringa oleifera extract has been reported to have anti-inflammatory and anti-oxidant properties. We have now examined the effects of Moringa oleifera Lam. on the depressed human T-cell responses, (IL-2 and IL-2 mRNA production) and DNA damage (quantifying the oxidized derivative of deoxyguanosine, 8-OHdG) induced oxidative stress. T-cells treated with oxidative substances, uric acid, aluminum chloride, hydrogen peroxide, and ultraviolet irradiation showed marked reduction in IL-2 production, which was prevented by pre-treating the cells with Moringa extract. These effects correlated with its prevention of the down-regulation of IL2 gene expression and a reduction in the DNA damage caused by oxidative stress. Thus the ability of Moringa extract to reduce inflammation is likely to relate to its ability to prevent T-cell hyporesponsiveness experienced in inflammatory diseases, through an action at the pre-transcriptional level.

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“…This may be in part due to chronic ultraviolet (UV) light exposure (Inoki et al 2004). UV may generate reactive oxygen species (ROS), contributing to oxidative stress (Wenk et al 2001). Since the cornea is the first target of UV-light entering the eye, it is especially susceptible to damage by ROS.…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms of the Apoptosis-Related FAS and FAS Ligand Genes in Keratoconus and Fuchs Endothelial Corneal Dystrophy

Synowiec

Wójcik

Izdebska

et al. 2014

Tohoku J. Exp. Med.

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Keratoconus (KC) is a non-inflammatory eye disease characterized by progressive corneal thinning and asymmetrical conical protrusion of the cornea. Fuchs endothelial corneal dystrophy (FECD) is a degenerative, slowly progressive disease of the corneal endothelium that is characterized by alteration in corneal endothelial cell morphology and progressive loss of these cells. They are unrelated eye diseases that may ultimately lead to vision loss. Their pathogenesis is largely unknown, although impaired apoptosis has been suggested to be responsible for both diseases. Therefore, we studied the frequency of the c.-671A>G polymorphism of the apoptosis-related FAS gene and the c.-844T>C polymorphism of the FAS ligand (FASLG) gene in patients with FECD (221 individuals) or KC (264) and controls (300). Each polymorphism is located within the putative cis-acting element of the respective promoter. Risk of KC or FECD was estimated with unconditional multiple logistic regression with adjustment for various factors, including age, sex, allergies, and family history. The T/T genotype and the T allele of the c.-844T>C polymorphism were associated with increased occurrence of KC, while the C allele was associated with decreased KC occurrence. The G allele of the c.-671A>G polymorphism was associated with increased occurrence of FECD, while the A allele was associated with decreased FECD occurrence. The C/C-A/A combined genotype was associated with reduced risk of FECD, whereas the T/T-G/A combined genotype increased risk of KC. In conclusion, variability in the expression of the FAS and FASLG genes may be involved in the pathogenesis of KC and FECD.

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UV-Induced Oxidative Stress and Photoaging

Cited by 194 publications

References 49 publications

DNA damage, death receptor activation and reactive oxygen species contribute to ultraviolet radiation-induced apoptosis in an essential and independent way

DNA damage, death receptor activation and reactive oxygen species contribute to ultraviolet radiation-induced apoptosis in an essential and independent way

Moringa Oleifera Lam. Leaves Extract Reduces Human T-Cell Hyporesponsiveness and Dna Damage Induced by Oxidative Stress

Polymorphisms of the Apoptosis-Related FAS and FAS Ligand Genes in Keratoconus and Fuchs Endothelial Corneal Dystrophy

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