Damaging Effects Of Light Research Articles

The protection of DNA in blood leukocytes from damaging action of ultraviolet radiation using the “Useful Sun” strategy

The damaging effects of light that was emitted by a DRSh250-3 mercury lamp on the DNA of mouse blood leukocytes was studied in vitro. It was shown that the main DNA damage is due to the action of UVB radiation (280–320 nm). Under the combined effects of the UV radiation and the orange–red fluorescent component it was found that the additional fluorescent light with the spectral maximum at 625 nm from nanoluminophore materials (quantum dots that are based on CdSe/ZnS, CdSe/CdS/ZnS) protected the cellular DNA from the damaging effect of UV radiation. Using nanomolar concentrations of hydrogen peroxide, the hypothesis of the role of reactive oxygen species in the protective effects of the red–orange light was tested in vitro. It was shown for the first time that the mechanisms of the protective effects are associated with the induction of an adaptive response by nanomolar concentrations of hydrogen peroxide that are induced by the orange–red light.

Structure and Conformation of the Carotenoids in Human Retinal Macular Pigment.

Human retinal macular pigment (MP) is formed by the carotenoids lutein and zeaxanthin (including the isomer meso-zeaxanthin). MP has several functions in improving visual performance and protecting against the damaging effects of light, and MP levels are used as a proxy for macular health–specifically, to predict the likelihood of developing age-related macular degeneration. While the roles of these carotenoids in retinal health have been the object of intense study in recent years, precise mechanistic details of their protective action remain elusive. We have measured the Raman signals originating from MP carotenoids in ex vivo human retinal tissue, in order to assess their structure and conformation. We show that it is possible to distinguish between lutein and zeaxanthin, by their excitation profile (related to their absorption spectra) and the position of their ν1 Raman mode. In addition, analysis of the ν4 Raman band indicates that these carotenoids are present in a specific, constrained conformation in situ, consistent with their binding to specific proteins as postulated in the literature. We discuss how these conclusions relate to the function of these pigments in macular protection. We also address the possibilities for a more accurate, consistent measurement of MP levels by Raman spectroscopy.

Blue light-absorbing intraocular lens and retinal pigment epithelium protection in vitro

Purpose: To compare the Alcon AcrySof® Natural (SN60AT) and AcrySof (SA60AT), the AMO Sensar® (AR40e) and ClariFlex®, and the Pfizer CeeOn® Edge 911A intraocular lenses (IOLs) as to their ability to protect retinal pigment epithelial (RPE) cells from light damage mediated by the lipofuscin fluorophore A2E. Setting: Department of Ophthalmology, Columbia University, New York, New York, USA. Methods: Cultured human RPE cells (ARPE-19 cell line) that had accumulated A2E were exposed to blue (430 nm ± 30), green (550 ± 10 nm), or white (390 to 750 nm) light with and without an IOL in the light path. Results: The blue light-absorbing AcrySof Natural IOL was associated with significant reduction (78% to 82%; P<.01) in the death of A2E-laden RPE that were exposed to blue, white, and green light. The decrease in the incidence of cell death was greater in magnitude than would be expected from the amount of light that was absorbed by the IOL. The considerably smaller declines in cell death observed with the AcrySof, Sensar, ClariFlex, and CeeOn Edge IOLs were likely due to nonspecific reductions in light transmittance. Conclusions: By absorbing blue light, the AcrySof Natural IOL shields RPE cells that have accumulated the aging lipofuscin fluorophore A2E from the damaging effects of light. A long-term population-based clinical trial would determine whether a blue light-absorbing IOL can reduce the risk for or progression of age-related macular degeneration.

Prostaglandin Postscript: A Personal Reflection

The long and arduous process that led to the development of ocular hypotensive prostaglandin derivatives over the past three decades has been reviewed several times. In this “postscript” to the second Survey of Ophthalmology supplement devoted to the ocular hypotensive effects of prostaglandin derivatives, only two aspects of this new approach to the medical management of glaucoma are discussed: 1) The implication of the observed prostaglandin-induced increase in iridial pigmentation with respect to the understanding of the role of prostaglandins and of iridial melanocytes in the protection against the damaging effects of light, and in the maintenance of normal intraocular microenvironment; and 2) The rationale behind the use of a combined formulation of a prostaglandin derivative and a beta-blocker for the protection against increased intraocular pressure. The need to consider not only target pressure, but also target mechanisms, in the selection of medical therapy regimen for any given glaucoma patient is emphasized.

Photochemical study of hexahydroquinoline derivatives--a new group of calcium antagonists.

The photochemical stability of 2,6,6-trimethyl-3-carbmethoxy-4-phenyl-5-oxo-1,4,5,6,7,8-hexahydroquinoline (HHQ) derivatives with different substituents on the phenyl ring (-Cl, -NO2, -CF3, -CH3, -OCH3) has been studied. The process of photodegradation was studied by UV spectrophotometry. The rate of photodegradation was found to depend on the type and position of the substituent in the phenyl ring. The compounds most susceptible to the damaging effect of light proved to be those containing the nitro group, in particular with the substituent in the ortho position of the aromatic ring. Derivatives with alkyl (-CH3) and halo-alkyl (-CF3) substituents showed the greatest photochemical stability. The compounds with substituents in the ortho position were found to be much less photostable than the meta isomers. The quantum yield values obtained ranged from 10(-4) to 10(-3), indicating the occurrence of secondary photochemical processes initiated by the primary products of decomposition.

Strategies for rescue of retinal photoreceptor cells

A variety of genetic and environmental factors cause degeneration of retinal photoreceptors. This review focuses on current strategies to rescue defective, but still viable, rods and cones, including transplantation of normal retinal pigment epithelium cells, corrective gene therapy, administration of survival/growth factors, protection from the damaging effects of light, and dietary supplementation of vitamin A.

Multiple growth factors, cytokines, and neurotrophins rescue photoreceptors from the damaging effects of constant light.

Recent demonstrations of survival-promoting activity by neurotrophic agents in diverse neuronal systems have raised the possibility of pharmacological therapy for inherited and degenerative disorders of the central nervous system. We have shown previously that, in the retina, basic fibroblast growth factor delays photoreceptor degeneration in Royal College of Surgeons rats with inherited retinal dystrophy and that the growth factor reduces or prevents the rapid photoreceptor degeneration produced by constant light in the rat. This light-damage model now provides an efficient way to assess quantitatively the survival-promoting activity in vivo of a number of growth factors and other molecules. We report here that photoreceptors can be significantly protected from the damaging effects of light by intravitreal injection of eight different growth factors, cytokines, and neurotrophins that typically act through several distinct receptor families. In addition to basic fibroblast growth factor, those factors providing a high degree of photoreceptor rescue include brain-derived neurotrophic factor, ciliary neurotrophic factor, interleukin 1 beta, and acidic fibroblast growth factor; those with less activity include neurotrophin 3, insulin-like growth factor II, and tumor necrosis factor alpha; those showing little or no protective effect are nerve growth factor, epidermal growth factor, platelet-derived growth factor, insulin, insulin-like growth factor I, heparin, and laminin. Although we used at least one relatively high concentration of each agent (the highest available), it is still possible that other concentrations or factor combinations might be more protective. Injecting heparin along with acidic fibroblast growth factor or basic fibroblast growth factor further enhanced the degree of photoreceptor survival and also suppressed the increased incidence of macrophages produced by either factor, especially basic fibroblast growth factor. These results now provide the impetus for determining the normal function in the retina, mechanism(s) of rescue, and therapeutic potential in human eye diseases for each agent.

Effectiveness of Vitamin E Protecting against UV‐Light — Comparative Testing of the Natural Tocopherols on the Skin of the Hairless Mouse

AbstractThe protective action of the natural d‐tocopherols d‐β, d‐γ and d‐δ‐tocopherol against the damaging effects of light was studied, and compared with that of d‐α‐tocopherol. The tests were carried out on hairless mice. The extent of edema formation caused by exposure to UV‐light was measured as a parameter for skin damage. The effectiveness of the d‐tocopherols was determined by subjecting the UV‐edema inhibition values to a special statistical procedure. It was proved that all natural d‐tocopherols inhibit skin edema after skin damage. The following activities were determined in comparison to d‐α‐tocopherol: d‐γ‐tocopherol 72%, d‐β‐tocopherol 42%, d‐δ‐tocopherol 40%. It was possible to exploit the properties of natural homologues as inhibitors of skin damage caused by exposure to UV‐light by using them as an auxiliary factor in the treatment of specific skin diseases and photodermatoses.

The Effect of Light on Textiles

The fading of dyes and tendering of fibres caused by exposure of dyed textiles to light is illustrated by work carried out at the Shirley Institute, and the importance of considering the fibre–dye–atmosphere system as a whole is emphasised. The same dyes differ in their effect on the photochemical degradation of cellulose acetate and nylon. Tendering of cotton is shown to be caused almost entirely by ultraviolet radiation, and the effect of light quality on fading and tendering is demonstrated. Tendering of vat‐dyed cotton on north‐ and south‐facing exposure is examined, and the behaviour of undyed and dyed cotton on indoor and outdoor exposure leads to the examination of the effects of atmospheric contaminants, particularly sulphur dioxide, in causing serious photochemical damage. Possible methods of protection from the damaging effects of light are discussed.