Retinal Sensitized Photodynamic Damage to Liposomes

Delmelle, M.

doi:10.1111/j.1751-1097.1978.tb07718.x

Cited by 61 publications

(35 citation statements)

References 21 publications

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“…Thus, one initial event may modify a large area of the membrane. This seems to correspond with a recent study of photodynamic damage to liposomes (Delmelle, 1978) which shows that photodynamic treatment results in an increase in the membrane fluidity and leads to lysis of the liposomes. It is quite possible that the bleb formation and swelling of the cells observed in the present study is a result of increased membrane fluidity.…”

Section: Molecular Mechanism Of Inactivationsupporting

confidence: 91%

The mechanism of photodynamic inactivation of human cells in vitro in the presence of haematoporphyrin

Moan¹,

Pettersen²,

Christensen³

1979

Br J Cancer

250

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Summary.-The photosensitizing effect of haematoporphyrin (HP) on human cells of the established line NHIK 3025 has been studied. Fluorescence measurements show that HP is bound to these cells. Serum proteins also bind HP, and the presence of 10% human serum during incubation with HP (3 x 10-4M) reduces the cellular uptake of HP by 75%o or more. The photosensitized inactivation is enhanced when the cells are suspended in D20-buffer during irradiation. This indicates that singlet oxygen is involved in the inactivation.Two findings indicate that the photoinduced damage is repairable: firstly, the fraction of cells surviving a given light dose decreases with decreasing irradiation temperature, and secondly, the survival curves have a shoulder at low exposures of light.

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Section: Molecular Mechanism Of Inactivationsupporting

confidence: 91%

The mechanism of photodynamic inactivation of human cells in vitro in the presence of haematoporphyrin

Moan¹,

Pettersen²,

Christensen³

1979

Br J Cancer

250

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“…Retinal, apart from being a reactive aldehyde, can also act as a photosensitizer (61,62), since its absorption spectrum (λ max ~380 nm) extends into the visible range. For the whole animal, the efficient clearance of retinal will be of particular relevance under bright light conditions when retinal will be generated continuously.…”

Section: Discussionmentioning

confidence: 99%

Interphotoreceptor Retinoid-Binding Protein Is the Physiologically Relevant Carrier That Removes Retinol from Rod Photoreceptor Outer Segments

Blakeley

Cornwall

et al. 2007

Biochemistry

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Light detection by vertebrate rod photoreceptor outer segments results in the destruction of the visual pigment, rhodopsin, as its retinyl moiety is photoisomerized from 11-cis to all-trans. The regeneration of rhodopsin is necessary for vision and begins with the release of the all-trans retinal and its reduction to all-trans retinol. Retinol is then transported out of the rod outer segment for further processing. We used fluorescence imaging to monitor retinol fluorescence and quantify the kinetics of its formation and clearance after rhodopsin bleaching in the outer segments of living isolated frog (Rana pipiens) rod photoreceptors. We independently measured the release of all-trans retinal from bleached rhodopsin in frog rod outer segment membranes and the rate of all-trans retinol removal by the lipophilic carriers interphotoreceptor retinoid binding protein (IRBP) and serum albumin. We find that the kinetics of all-trans retinol formation in frog rod outer segments after rhodopsin bleaching are to a good first approximation determined by the kinetics of all-trans retinal release from the bleached pigment. For the physiological concentrations of carriers, the rate of retinol removal from the outer segment is determined by the IRBP concentration, while the effect of serum albumin is negligible. The results indicate the presence of a specific interaction between IRBP and rod outer segment, probably mediated by a receptor. The effect of different concentrations of IRBP on the rate of retinol removal shows no cooperativity and has an EC 50 of 40 μmol/L.The vertebrate cells responsible for vision are the rod and cone photoreceptors of the retina that convert incoming light to an electrical signal. This conversion takes place in the photoreceptor outer segments, which are full of membrane disks containing the visual pigment, and, in a physiologically important arrangement, are enveloped by the retinal pigment epithelium (RPE). The visual pigment is composed of a chromophore, 11-cis retinal, attached to an integral membrane protein, opsin. The detection of light begins with the absorption of incoming photons by the visual pigment. An absorbed photon isomerizes the chromophore † Supported by NIH/NEI grants EY14850 (YK), EY04939 (RKC) , NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript moiety from 11-cis to all-trans bringing about a conformational change that initiates a cascade of reactions culminating in membrane potential change. The recovery of the cell from light involves the deactivation of the intermediates activated by light, and the reestablishment of membrane potential (1,2). However, the isomerized chromophore, all-trans retinal, remains. For vision to be possible, it is essential that the visual pigment regenerate: that is, the alltrans retinal has to be removed, and fresh 11-cis retinal has to be provided to combine with opsin and reform the visual pigment. The reactions regenerating the pigment are known as the Visual Cycle (3-5).In the case of the rod photoreceptors, t...

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“…55,75,180 Finally, the process of phagocytosis by the RPE is itself an oxidative stress and results in the generation of ROI.…”

Section: Generation Of Reactive Oxygen Intermediates In the Retinamentioning

confidence: 99%

The Role of Oxidative Stress in the Pathogenesis of Age-Related Macular Degeneration

Beatty

Koh²,

Phil

et al. 2000

Survey of Ophthalmology

1,772

1,347

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Abstract. Age-related macular degeneration (AMD) is the leading cause of blind registration in the developed world, and yet its pathogenesis remains poorly understood. Oxidative stress, which refers to cellular damage caused by reactive oxygen intermediates (ROI), has been implicated in many disease processes, especially age-related disorders. ROIs include free radicals, hydrogen peroxide, and singlet oxygen, and they are often the byproducts of oxygen metabolism. The retina is particularly susceptible to oxidative stress because of its high consumption of oxygen, its high proportion of polyunsaturated fatty acids, and its exposure to visible light. In vitro studies have consistently shown that photochemical retinal injury is attributable to oxidative stress and that the antioxidant vitamins A, C, and E protect against this type of injury. Furthermore, there is strong evidence suggesting that lipofuscin is derived, at least in part, from oxidatively damaged photoreceptor outer segments and that it is itself a photoreactive substance. However, the relationships between dietary and serum levels of the antioxidant vitamins and age-related macular disease are less clear, although a protective effect of high plasma concentrations of ␣ -tocopherol has been convincingly demonstrated. Macular pigment is also believed to limit retinal oxidative damage by absorbing incoming blue light and/or quenching ROIs. Many putative risk-factors for AMD have been linked to a lack of macular pigment, including female gender, lens density, tobacco use, light iris color, and reduced visual sensitivity. Moreover, the Eye Disease Case-Control Study found that high plasma levels of lutein and zeaxanthin were associated with reduced risk of neovascular AMD. The concept that AMD can be attributed to cumulative oxidative stress is enticing, but remains unproven. With a view to reducing oxidative damage, the effect of nutritional antioxidant supplements on the onset and natural course of age-related macular disease is currently being evaluated. Age-related macular degeneration (AMD) is the leading cause of blind registration in the western world, 119 and its prevalence is likely to rise as a consequence of increasing longevity. 225 There is a general consensus that cumulative oxidative damage is responsible for aging, and may, therefore, play an important role in the pathogenesis of AMD. In this article, we review the literature germane to oxidative processes in the retina and examine the evidence for a causal link between oxidative stress and age-related macular degeneration.

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Retinal Sensitized Photodynamic Damage to Liposomes

Cited by 61 publications

References 21 publications

The mechanism of photodynamic inactivation of human cells in vitro in the presence of haematoporphyrin

The mechanism of photodynamic inactivation of human cells in vitro in the presence of haematoporphyrin

Interphotoreceptor Retinoid-Binding Protein Is the Physiologically Relevant Carrier That Removes Retinol from Rod Photoreceptor Outer Segments

The Role of Oxidative Stress in the Pathogenesis of Age-Related Macular Degeneration

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