Effects of antioxidant nutrient deficiency on the retina and retinal pigment epithelium of albino rats: a light and electron microscopic study

Katz, Martin L.; Parker, K.R.; Handelman, Garry J.; Bramel, Terri L.; Dratz, Edward A.

doi:10.1016/0014-4835(82)90082-3

Cited by 105 publications

(30 citation statements)

References 36 publications

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“…When taken up by the endothelial cells of pigment epithelium choriocapillaries and the microvasculature of the inner portion of the retina, they produce structural damage to the blood-retina barrier, and particularly to the photoreceptor layer where peroxidase is absent [19]. The membrane structural integrity could be strikingly damaged by substantial peroxidation as seen by the loss of disk membrane morphology under the electron microscope [20,21]. Moreover, AT inhibition essentially brings about an accumulation of highly cytotoxic lysophospholipids, the products of activated phospholipases [16,22].…”

Section: Discussionmentioning

confidence: 99%

Susceptibility of rat retina acyl‐CoA: 1‐acyl‐sn‐glycero‐3‐phosphocholine O‐acyltransferase and CTP:phosphocholine cytidylyltransferase activity to lipid peroxidation and hydroperoxide treatment

et al. 1994

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AhShCtTwo enzyme activities involved in phospholipid metabolism in the rat retina were determined after in vivo and in vitro peroxidation according to several model systems. The in vivo models were based on: (i) intravenous administration of a sonicated emulsion of phospholipid and linoleate photooxidized mixture to normal rat for a period of one week; (ii) acute injection of Fe" solution (20 mMJ or (iii) 0.5 mg of hydroperoxylinoleate into the vitreous body, and collection of retinal tissue 4 h or 4 days later, respectively. Oleoyl CoAzlysophosphatidylcholine acyltransferase activity was unchanged or exhibited significant inhibition. On the contrary, CTF?phosphocholine cytidylyltransferase activity was stimulated. By incubating in vitro the retina with: (i) Fe*'-ascorbate; (ii) photooxidized phospholipid mixture (0.1-5 mM) or individual phospholipid classes; (iii) hydroperoxylinoleate (0.25-2 mM), with or without Fe*', a significant inactivation of acyltransferase (six-fold maximum loss of initial activity) and a slight stimulation of cytidylyltransferase were seen. Altogether, the results suggest that in situ oxygen radical generation by a variety of agents irreversibly perturbs enzymes and/or membrane structures in which the enzymes are inserted; these events may be a causal factor in retinal degeneration accompanying some ocular diseases.

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Section: Discussionmentioning

confidence: 99%

Susceptibility of rat retina acyl‐CoA: 1‐acyl‐sn‐glycero‐3‐phosphocholine O‐acyltransferase and CTP:phosphocholine cytidylyltransferase activity to lipid peroxidation and hydroperoxide treatment

et al. 1994

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“…Further, studies have elucidated the potential benefit of vitamin and antioxidant supplementation to reduce light-induced damage. 77,131,[135][136][137][138][139] Zeaxanthin, meso-zeaxanthin, and lutein are dietary carotenoids, which together form macular pigment and are thought to provide protection against oxidative damage. Owing to their molecular nature, the macular pigments are able to use their high number of double bonds to neutralize singlet oxygen, free radicals, and triple state photosensitizers, and thereby limit lipid membrane peroxidation.…”

Section: Variables In Photochemical Injurymentioning

confidence: 99%

Retinal light toxicity

Youssef

Sheibani

Albert

2010

Eye

271

204

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The ability of light to enact damage on the neurosensory retina and underlying structures has been well understood for hundreds of years. While the eye has adapted several mechanisms to protect itself from such damage, certain exposures to light can still result in temporal or permanent damage. Both clinical observations and laboratory studies have enabled us to understand the various ways by which the eye can protect itself from such damage. Light or electromagnetic radiation can result in damage through photothermal, photomechanical, and photochemical mechanisms. The following review seeks to describe these various processes of injury and many of the variables, which can mitigate these modes of injury.

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“…The brain slices were incubated in the fixative for at least two hours at room temperature with gentle agitation. Small regions of the cerebral cortex and cerebellar cortex were then dissected and processed for electron microscopy (Katz et al, 1982). Retina samples were prepared for electron microscopy as described previously (Lei et al, 2006).…”

Section: Assessment Of Storage Materials Accumulation In Brain and Retinamentioning

confidence: 99%

Phenotypic characterization of a mouse model of juvenile neuronal ceroid lipofuscinosis

Katz

Johnson

Tullis

2008

Neurobiology of Disease

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Juvenile neuronal ceroid lipofuscinosis (JNCL) is an autosomal recessively inherited neurodegenerative disorder that results from mutations in the CLN3 gene. JNCL is characterized by accumulation of autofluorescent lysosomal storage bodies, vision loss, seizures, progressive cognitive and motor decline, and premature death. Studies were undertaken to characterize the neuronal ceroid lipofuscinosis phenotype in a Cln3 knockout mouse model. Progressive accumulation of autofluorescent storage material was observed in brain and retina of affected mice. The Cln3 -/-mice exhibited progressively impaired inner retinal function, altered pupillary light reflexes, losses of inner retinal neurons, and reduced brain mass. Behavioral changes included reduced spontaneous activity levels and impaired learning and memory. In addition, Cln3 -/-mice had significantly shortened life spans. These phenotypic features indicate that the mouse model will be useful for investigating the mechanisms underlying the disease pathology in JNCL and provide quantitative markers of disease pathology that can be used for evaluating the efficacies of therapeutic interventions.

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Effects of antioxidant nutrient deficiency on the retina and retinal pigment epithelium of albino rats: a light and electron microscopic study

Cited by 105 publications

References 36 publications

Susceptibility of rat retina acyl‐CoA: 1‐acyl‐sn‐glycero‐3‐phosphocholine O‐acyltransferase and CTP:phosphocholine cytidylyltransferase activity to lipid peroxidation and hydroperoxide treatment

Susceptibility of rat retina acyl‐CoA: 1‐acyl‐sn‐glycero‐3‐phosphocholine O‐acyltransferase and CTP:phosphocholine cytidylyltransferase activity to lipid peroxidation and hydroperoxide treatment

Retinal light toxicity

Phenotypic characterization of a mouse model of juvenile neuronal ceroid lipofuscinosis

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