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L M Rapp

Publications and source records attributed to L M Rapp.

30 records · Page 2Linked to original sources
PubMed1986

Polyunsaturated fatty acids and vitamin E in rat rod outer segments during light damage.

Previous evidence suggests that lipid peroxidation may initiate photoreceptor damage induced by constant light exposure. In order to investigate the role of the antioxidant vitamin E in light damage, Long-Evans (pigmented) rats were atropinized and exposed to constant fluorescent light (Vita-Lite) of 10-20 foot candles for intervals up to 5 days. Following light exposure, retinal rod outer segments (ROS) were prepared and their lipids extracted. Retinas processed in parallel for morphological examination showed progressive ROS deterioration and selective loss of photoreceptor cells at 3 and 5 days of constant light. Similar to previous observations in undilated albino rats, constant illumination resulted in the specific loss of docosahexaenoic acid (22:6 omega 3) in the ROS. A novel finding in this study was an increase in the content of vitamin E relative to lipid phosphorus, stearic acid, and docosahexaenoic acid in the ROS of constant light-exposed animals.

Animals↗
PubMed1985

DNA repair synthesis in the rat retina following in vivo exposure to 300-nm radiation.

Quantitative autoradiography was used to study the incorporation of 3H-thymidine into the retina of albino rats following in vivo exposure to 300-nm radiation. Relative to background labeling in unexposed eyes, there was 8-20 times as much label per unit area in the outer nuclear layer, inner nuclear layer, and ganglion cells of 300-nm exposed retinas. The photoreceptor inner segments also showed thymidine labeling in both control and exposed retinas.

Animals↗
PubMed1984

Lipid peroxidation and retinal degeneration.

Retinal degenerations were produced in albino rats by exposure to constant illumination or in frogs and albino rats by intravitreal injections of ferrous sulfate. Both treatments resulted in the loss of long-chain polyunsaturated fatty acids and the accumulation of lipid hydroperoxides in isolated rod outer segments. We suggest that lipid peroxidation is a factor in certain types of retinal degenerations.

Animals↗
PubMed1983

Evidence for rod outer segment lipid peroxidation following constant illumination of the rat retina.

Constant illumination for three days (100-125 foot-candles) caused degeneration of photoreceptor cells in the albino rat retina and was accompanied by a reduction in the levels of docosahexaenoic acid (22:6 omega 3), the major polyunsaturated fatty acid in rod outer segments (ROS). An increase in the level of lipid conjugated dienes, a measure of lipid hydroperoxides, also was observed in ROS after 24-72 hours of constant illumination. These data support the suggestion that peroxidation of long-chain polyunsaturated fatty acids in ROS may be a factor in light-induced retinal degeneration.

Animals↗
PubMed1982

The effects of local anaesthetics on retinal function.

Isolated frog eyecups were incubated in Ringer containing local anaesthetics to study the effects of these drugs on dark-adaptation of the ERG. Relative to controls, dark-adaptation in eyecups treated with millimolar concentrations of MS-222, benzocaine, and procaine HCl was significantly inhibited during 10 to 120 min following the cessation of the adapting light. These drugs also prevented the recovery of the c-wave during dark-adaptation, resulting in ERG waveforms resembling those found in light-adapted eyecups. Measurements of rhodopsin in the retina were consistent with previous findings showing that rhodopsin regeneration in situ is inhibited by local anaesthetics. In vitro regeneration experiments in which bleached rod outer segment fragments were added to 11-cis retinal showed that preincubation of retinal with MS-222 in ethanol prevents rhodopsin regeneration. Evidence was obtained spectrophotometrically for the formation of a complex between MS-222 and 11-cis retinal with a gamma max of 512 nm. We propose that the formation of a Schiff's base between these two compounds blocks the recombination of rhodopsin, and in situ, leads to the inhibition of dark-adaptation.

Aminobenzoates↗
PubMed1982

Distribution of melanosomes across the retinal pigment epithelium of a hooded rat: implications for light damage.

Distribution of melanosomes across the retinal pigment epithelium of hooded rats (Long-Evans) is studied at the light microscopic and electron microscopic levels. This distribution is shown to be nonuniform: more melanosomes exist in the periphery than elsewhere and, importantly, there are very few melanosomes in a restricted area of the central portion of the superior hemisphere compared with the corresponding part of the inferior hemisphere. The region with fewest melanosomes is precisely the one that is highly susceptible to light damage. Because this region is the same in both pigmented and albino eyes, the paucity of melanin in this region is not the cause of its great sensitivity to light damage. Nor does light cause the nonuniform distribution of melanin. A possible explanation, involving a proposed vestigial tapetum, is given in order to explain the correlation of melanosome counts and sensitivity to light damage.

Animals↗
PubMedDate not supplied

Photoreceptor-specific degeneration caused by tunicamycin.

The antibiotic tunicamycin inhibits the biosynthesis of N-acetylglucosaminylpyrophosphoryl polyisoprenol, a key intermediate in the formation of the asparagine-linked oligosaccharides of glycoproteins. The effects of tunicamycin have been studied in various biological systems, primarily with the aim of elucidating the role of the carbohydrate moieties in the cellular function of glycoproteins. Rhodopsin, the visual pigment of retinal rod photoreceptor cells, is a membrane glycoprotein which consists of a single polypeptide chain (opsin) to which a chromophoric prosthetic group (II-cis-retinaldehyde) and two asparagine-linked oligosaccharide chains are covalently attached. The glycosylation of opsin can be blocked with tunicamycin in vitro in conditions where polypeptide synthesis is only slightly decreased. We have reported that tunicamycin can disrupt the normal assembly of rod outer segment membranes in vitro without significantly inhibiting the biosynthesis or intracellular transport of opsin. Here we report that intraocular injection of tunicamycin produces a photoreceptor-specific degeneration characterized by progressive shortening of rod outer segment, decreased membrane assembly, and eventual photoreceptor cell death.

Animals↗