UVB‐induced formation of (6–4) photoproducts in the rat corneal epithelium

Estil, Svein; Olsen, Wenche Marie; Huitfeldt, Henrik S.; Haaskjold, Erling

doi:10.1111/j.1600-0420.1997.tb00104.x

Cited by 14 publications

(5 citation statements)

References 38 publications

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“…These finding are consistent with earlier studies showing 6-4 PPs in rat corneas exposed to as little as 25 mJ/ cm 2 of UV-B. 41 Similarly, CPDs were induced by UV-B exposure of the rabbit cornea. 42 Corneal transmittance determines the potential impact of UV-B on intraocular tissues such as the lens.…”

Section: Discussionsupporting

confidence: 93%

UV-B–Induced DNA Damage and Repair in the Mouse Lens

Mesa¹,

Bassnett²

2013

Invest. Ophthalmol. Vis. Sci.

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Even relatively modest exposures to UV-B produced 6-4 PP and CPD photolesions in lens epithelial cells. Cyclobutane pyrimidine dimer lesions were particularly prevalent and were repaired slowly if at all. Studies on sun-exposed skin have established a causal connection between photolesions and so-called UV-signature mutations. If similar mechanisms apply in the lens, it suggests that somatic mutations in lens epithelial cells may contribute to the development of cortical cataracts.

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Section: Discussionsupporting

confidence: 93%

UV-B–Induced DNA Damage and Repair in the Mouse Lens

Mesa¹,

Bassnett²

2013

Invest. Ophthalmol. Vis. Sci.

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“…Oxidative stress induced by UVB in the ocular surface epithelium upregulates the expression of proinflammatory cytokines (e.g., IL-1, IL-6, and IL-8, through the c-jun amino-terminal kinase [JNK] pathway, p38 pathway, and nuclear factor–kB [NF-kB] pathway) and enzymes (e.g. MMP-1) that mediate prostaglandin and leukotriene biosynthesis, as well as antioxidant enzymes in corneal epithelial cells [ 27 – 31 ]. These findings suggest that UV light can induce inflammation and tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Influence of Light Emitting Diode-Derived Blue Light Overexposure on Mouse Ocular Surface

Lee

Cui

et al. 2016

PLoS ONE

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PurposeTo investigate the influence of overexposure to light emitting diode (LED)-derived light with various wavelengths on mouse ocular surface.MethodsLEDs with various wavelengths were used to irradiate C57BL/6 mice at an energy dose of 50 J/cm2, twice a day, for 10 consecutive days. The red, green, and blue groups represented wavelengths of 630 nm, 525 nm, and 410 nm, respectively. The untouched group (UT) was not exposed to LED light and served as the untreated control. Tear volume, tear film break-up time (TBUT), and corneal fluorescein staining scores were measured on days 1, 3, 5, 7, and 10. Levels of interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were measured in the cornea and conjunctiva using a multiplex immunobead assay at day 10. Levels of malondialdehyde (MDA) were measured with an enzyme-linked immunosorbent assay. Flow cytometry, 2’7’-dichlorofluorescein diacetate (DCF-DA) assay, histologic analysis, immunohistochemistry with 4-hydroxynonenal, and terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) staining were also performed.ResultsTBUT of the blue group showed significant decreases at days 7 and 10, compared with the UT and red groups. Corneal fluorescein staining scores significantly increased in the blue group when compared with UT, red, and green groups at days 5, 7, and 10. A significant increase in the corneal levels of IL-1β and IL-6 was observed in the blue group, compared with the other groups. The blue group showed significantly increased reactive oxygen species production in the DCF-DA assay and increased inflammatory T cells in the flow cytometry. A significantly increased TUNEL positive cells was identified in the blue group.ConclusionsOverexposure to blue light with short wavelengths can induce oxidative damage and apoptosis to the cornea, which may manifest as increased ocular surface inflammation and resultant dry eye.

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“…The corneal epithelium serves as a protective barrier, absorbing UVB light and minimizing damage to the interior eye including the lens and retina. However, in excessive amounts, UVB light can injure the cornea, a process that causes aberrant epithelial cell growth and differentiation, as well as cell death via necrosis and apoptosis [3, 4]. This can result in corneal opacities or photokeratitis [5-7].…”

Section: Introductionmentioning

confidence: 99%

UVB light regulates expression of antioxidants and inflammatory mediators in human corneal epithelial cells

Black

Gordon

Heck

et al. 2011

Biochemical Pharmacology

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The cornea is highly sensitive to ultraviolet B (UVB) light-induced oxidative stress, a process that results in the production of inflammatory mediators which have been implicated in tissue injury. In the present studies, we characterized the inflammatory response of human corneal epithelial cells to UVB (2.5 - 25 mJ/cm2). UVB caused a dose-dependent increase in the generation of reactive oxygen species in the cells. This was associated with increases in mRNA expression of the antioxidants Cu,Zn superoxide dismutase (SOD), Mn-SOD, catalase and heme oxygenase-1 (HO-1), as well as the glutathione S-transferases (GST), GSTA1-2, GSTA3, GSTA4, GSTM1, mGST2. UVB also upregulated expression of the proinflammatory cytokines, IFNγ, IL-1β, TGFβ and TNFα, and enzymes important in prostaglandin (PG) biosynthesis including cyclooxygenase-2 (COX-2) and the PG synthases mPGES-2, PGDS, PGFS and thromboxane synthase, and in leukotriene biosynthesis including 5-lipoxygenase (5-LOX), and the epidermal and platelet forms of 12-LOX and 15-LOX-2. UVB was found to activate JNK and p38 MAP kinases in corneal epithelial cells; ERK1/2 MAP kinase is constitutively active, but its activity was increased following UVB treatment. Inhibition of p38 blocked UVB-induced expression of TNFα, COX-2, PGDS and 15-LOX-2, while JNK inhibition suppressed TNFα and HO-1. These data indicate that UVB modulates corneal epithelial cell expression of antioxidants and proinflammatory mediators by distinct mechanisms. Alterations in expression of these mediators are likely to be important in regulating inflammation and protecting the cornea from UVB-induced oxidative stress.

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UVB‐induced formation of (6–4) photoproducts in the rat corneal epithelium

Cited by 14 publications

References 38 publications

UV-B–Induced DNA Damage and Repair in the Mouse Lens

UV-B–Induced DNA Damage and Repair in the Mouse Lens

Influence of Light Emitting Diode-Derived Blue Light Overexposure on Mouse Ocular Surface

UVB light regulates expression of antioxidants and inflammatory mediators in human corneal epithelial cells

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