11-cis-retinal and Vitamin-A-Deficiency

Vitamin A refers collectively to a number of compounds, the most biologically active of which is retinol. Named after its earliest discovered function, visual excitation, retinol is also needed for growth and reproduction, and differentiation of epithelial tissue. A closely related form, retinoic acid, has selective biologic activity for normal growth and epithelial differentiation. The term retinoids has been used in recent years to include both natural and synthetic analogs of vitamin A. Carotene and carotenoids refer to vitamin A precursors (pro-vitamins) of vegetable origin. Following a brief historical account of vitamin A and description of dietary information this article focuses on the chemistry and physiology of retinoids. The biological roles of vitamin A compounds are elaborated, as well as the clinical significance of vitamin A deficiency and excess. Discussion of retinoids in therapy includes their use as anti-cancer agents and as therapeutics for dermatological disorders. Finally, a review of analytical techniques for laboratory assessment of vitamin A is presented.

Topics: Adult; Animals; Antineoplastic Agents; Carcinogens; Carotenoids; Chemical and Drug Induced Liver Injury; Chemical Phenomena; Chemistry; Female; Humans; Hypervitaminosis A; Infant; Male; Pregnancy; Rhodopsin; Tretinoin; Vitamin A; Vitamin A Deficiency

Topics: Chromosome Aberrations; Chromosome Disorders; Cyclic GMP; Electroretinography; Female; Humans; Photoreceptor Cells; Retina; Retinitis Pigmentosa; Rhodopsin; Sex Chromosome Aberrations; Vision Disorders; Vitamin A Deficiency; X Chromosome

Insufficient dietary intake of vitamin A causes various human diseases. For instance, chronic vitamin A deprivation causes blindness, slow growth, impaired immunity, and an increased risk of mortality in children. In contrast to these diverse effects of vitamin A deficiency (VAD) in mammals, chronic VAD in flies neither causes obvious developmental defects nor lethality. As in mammals, VAD in flies severely affects the visual system: it impairs the synthesis of the retinal chromophore, disrupts the formation of the visual pigments (Rhodopsins), and damages the photoreceptors. However, the molecular mechanisms that respond to VAD remain poorly understood. To identify genes and signaling pathways that are affected by VAD, we performed RNA-sequencing and differential gene expression analysis in Drosophila melanogaster. We found an upregulation of genes that are essential for the synthesis of the retinal chromophore, specific aminoacyl-tRNA synthetases, and major nutrient reservoir proteins. We also discovered that VAD affects several genes that are required for the termination of the light response: for instance, we found a downregulation of both arrestin genes that are essential for the inactivation of Rhodopsin. A comparison of the VAD-responsive genes with previously identified blue light stress-responsive genes revealed that the two types of environmental stress trigger largely nonoverlapping transcriptome responses. Yet, both stresses increase the expression of seven genes with poorly understood functions. Taken together, our transcriptome analysis offers insights into the molecular mechanisms that respond to environmental stresses.

Topics: Animals; Drosophila melanogaster; Drosophila Proteins; Gene Expression; Rhodopsin; Vitamin A; Vitamin A Deficiency

To characterize the influence of light and vitamin A on retinal degeneration in an animal model of retinitis pigmentosa caused by the rhodopsin P23H mutation.. Retinal degeneration was examined in transgenic Xenopus laevis expressing P23H rhodopsin, in which retinal degeneration is completely rescued by preventing light exposure. The sensitivity of this retinal degeneration to varying intensities, wavelengths, and durations of light exposure, and to vitamin A deprivation was characterized.. Green light was the most effective inducer of retinal degeneration in this model. Retinal degeneration was induced by prolonged exposure to green light and was prevented by filters that block short wavelengths. Reducing the duration of light exposure prevented retinal degeneration, even when the light intensity was proportionally increased. Vitamin A deprivation also induced retinal degeneration associated with defects in P23H rhodopsin biosynthesis. Vitamin A deprivation did not cause retinal degeneration in nontransgenic animals.. The mechanism of retinal degeneration in this animal model of RP involves the interaction of light with rhodopsin rather than with free chromophore or bleached rhodopsin. These results may explain the clinical benefits of vitamin A for patients with retinitis pigmentosa and may indicate that pharmacological chaperones are a viable approach to RP therapy. Results also suggest strategies for minimizing RD in patients through controlling light exposure duration or wavelengths.

Topics: Animals; Animals, Genetically Modified; Light; Male; Microscopy, Confocal; Mutation, Missense; Photometry; Radiation Injuries, Experimental; Retina; Retinal Degeneration; Rhodopsin; Transgenes; Vitamin A; Vitamin A Deficiency; Xenopus laevis

Accumulation of free opsin by mutations in rhodopsin or insufficiencies in the visual cycle can lead to retinal degeneration. Free opsin activates phototransduction; however, the link between constitutive activation and retinal degeneration is unclear. In this study, the photoresponses of Xenopus rods rendered constitutively active by vitamin A deprivation were examined. Unlike their mammalian counterparts, Xenopus rods do not degenerate. Contrasting phototransduction in vitamin A-deprived Xenopus rods with phototransduction in constitutively active mammalian rods may provide new understanding of the mechanisms that lead to retinal degeneration.. The photocurrents of Xenopus tadpole rods were measured with suction electrode recordings, and guanylate cyclase activity was measured with the IBMX (3-isobutyl-1-methylxanthine) jump technique. The amount of rhodopsin in rods was determined by microspectrophotometry.. The vitamin A-deprived rod outer segments were 60% to 70% the length and diameter of the rods in age-matched animals. Approximately 90% of its opsin content was in the free or unbound form. Analogous to bleaching adaptation, the photoresponses were desensitized (10- to 20-fold) and faster. Unlike bleaching adaptation, the vitamin A-deprived rods maintained near normal saturating (dark) current densities by developing abnormally high rates of cGMP synthesis. Their rate of cGMP synthesis in the dark (15 seconds(-1)) was twofold greater than the maximum levels attainable by control rods ( approximately 7 seconds(-1)).. Preserving circulating current density and response range appears to be an important goal for rod homeostasis. However, the compensatory changes associated with vitamin A deprivation in Xenopus rods come at the high metabolic cost of a 15-fold increase in basal ATP consumption.

Topics: Animals; Calbindins; Cyclic GMP; Dark Adaptation; Electrophysiology; Fluorescent Antibody Technique, Indirect; Guanylate Cyclase; Hydrolysis; Light; Microspectrophotometry; Photic Stimulation; Retinal Degeneration; Retinal Rod Photoreceptor Cells; Rhodopsin; S100 Calcium Binding Protein G; Vision, Ocular; Vitamin A Deficiency; Xenopus laevis

Visual pigments (rhodopsins) are composed of a chromophore (vitamin A derivative) bound to a protein moiety embedded in the retinal membranes. Animals cannot synthesize the visual chromophore de novo but rely on the uptake of carotenoids, from which vitamin A is formed enzymatically by oxidative cleavage. Despite its importance, the enzyme catalyzing the key step in vitamin A formation resisted molecular analyses until recently, when the successful cloning of a cDNA encoding an enzyme with beta,beta-carotene-15,15'-dioxygenase activity from Drosophila was reported. To prove its identity with the key enzyme for vitamin A formation in vivo, we analyzed the blind Drosophila mutant ninaB. In two independent ninaB alleles, we found mutations in the gene encoding the beta,beta-carotene-15,15'-dioxygenase. These mutations lead to a defect in vitamin A formation and are responsible for blindness of these flies.

Topics: Amino Acid Sequence; Amino Acid Substitution; Animals; Base Sequence; beta-Carotene 15,15'-Monooxygenase; Blindness; Chickens; Cloning, Molecular; Crosses, Genetic; Drosophila melanogaster; Drosophila Proteins; Female; Heterozygote; Humans; Male; Molecular Sequence Data; Mutagenesis, Site-Directed; Mutation; Oxygenases; Point Mutation; Recombinant Proteins; Reverse Transcriptase Polymerase Chain Reaction; Rhodopsin; RNA, Messenger; Sequence Alignment; Sequence Homology, Amino Acid; Vitamin A; Vitamin A Deficiency

Photoreceptive membranes of Drosophila compound eyes were studied by quick-freezing electron microscopy. The quick-frozen photoreceptive microvilli appeared cylindrical in shape either when they were freeze-substituted or freeze-fractured. Deep-etch replication revealed the extracellular surfaces of microvilli which were covered by various particles arranged in a helical manner. The protoplasmic surfaces were covered by more regular helical rows of particles about 10 nm in diameter. When rhodopsin content of the photoreceptive membranes was reduced by vitamin A-deficiency, the intramembrane particles drastically decreased resulting in the disappearance of particles in rows. Our results strongly suggest the regular arrangement of rhodopsin molecules in invertebrate photoreceptive membranes.

Topics: Animals; Drosophila melanogaster; Freeze Etching; Freeze Fracturing; Microscopy, Electron; Microvilli; Photoreceptor Cells; Rhodopsin; Vitamin A Deficiency

Dietary deficiency in the retinoid precursors of the visual pigment chromophore 11-cis retinal eventually results in selective degeneration of the photoreceptor cells of the vertebrate retina. An early effect of retinoid deficiency is depletion of chromophore from the photoreceptor outer segments. Experiments were conducted to determine whether the rate of chromophore depletion was affected by the intensity of environmental light.. Rats were maintained on diets either containing or lacking retinoid precursors of 11-cis retinal for up to 30 weeks. Animals in both dietary groups were exposed to either bright (90 lux) or dim (5 lux) cyclic light for the duration of the experiment. At various time intervals retinal rhodopsin content and photoreceptor densities were determined in animals from each treatment group.. Bright light greatly accelerated the depletion of rhodopsin from the retina. Rhodopsin was almost completely depleted from the retinas of the retinoid-deficient animals raised under bright light for 25 weeks, whereas the dim-light-reared animals fed the retinoid-deficient diet still had significant amounts of retinal rhodopsin even after 30 weeks. Bright light alone moderately depressed retinal rhodopsin levels in animals fed the diet containing a vitamin A precursor of 11-cis retinal. Among rats fed the latter diet, retinal rhodopsin content in the animals kept in bright cyclic light was maintained throughout the experiment at about 70% of the amount of rhodopsin in rats housed in dim cyclic light. The light-related rhodopsin depletion in the retinoid-deprived rats was accompanied by photoreceptor cell death. After 30 weeks of treatment, photoreceptor cell densities remained similar in all treatment groups except the retinoid-deprived group housed under bright cyclic light. In the latter group, photoreceptor cell densities in the central retinas were reduced by an average of more than 50% after 30 weeks. Retinoid deficiency and bright light exposure alone each resulted in a reduction in rod outer segment size. An even greater reduction in outer segment size was observed in vitamin A-deprived animals housed under bright cyclic light.. These findings indicate that light accelerates the depletion of retinoids from the retina and the accompanying photoreceptor cell degeneration.

Topics: Animals; Cell Count; Cell Death; Dark Adaptation; Diet; Disease Models, Animal; Light; Male; Photoreceptor Cells; Rats; Rats, Inbred F344; Retinal Degeneration; Rhodopsin; Rod Cell Outer Segment; Vitamin A; Vitamin A Deficiency

Dietary deficiency in the retinoid precursors of the visual pigment chromophore 11-cis retinal results in the synthesis of photoreceptor outer segments containing opsin in excess of the vitamin A available for rhodopsin regeneration. This suggests that vitamin A-free opsin may be incorporated into newly synthesized outer segment disc membranes. If this opsin is functionally intact, it should be possible convert it to rhodopsin in vivo by providing the appropriate retinoids, and the resulting rhodopsin should should be able to mediate visual transduction. Experiments were conducted to evaluate this possibility and to identify the rate-limiting steps in photoreceptor recovery from retinoid depletion. Rates were maintained on diets either containing or lacking retinoid precursors of 11-cis retinal for 23 weeks, at which time outer segment opsin content greatly exceeded the availability of visual cycle retinoids in the retina. The retinoid-deprived animals were then each given a single intramuscular injection of all-trans retinol. At various time intervals after retinol administration, electroretinograms (ERGs) were recorded on some rats, and retinal rhodopsin contents were determined in others. At similar time intervals, blood and retinal pigment epithelial (RPE) retinoid levels and photoreceptor outer segment size were also determined. No significant increase in retinal rhodopsin content was observed up to 8 hr after injection, despite the fact that by 3 hr, blood retinol levels had recovered to more than 30% of normal. By 1 day after injection, however, rhodopsin levels had recovered to 30% of normal and ERG responses showed increases in visual sensitivity commensurate with the recovery of rhodopsin. The lag in rhodopsin recovery was apparently due to delayed uptake of retinol from the blood by the RPE. Photoreceptor outer segment size was reduced by over 50% in the retinoid- deprived rats and did not begin to recover by 1 day. By 1 week, however, outer segment size had returned to an average of 65% of normal. Commensurate with this regrowth of the outer segments, both rhodopsin levels and visual sensitivity increased between 1 and 7 days after vitamin A administration. Because the rates of recovery in rhodopsin levels and visual sensitivity greatly exceeded the normal rate of new opsin synthesis at short time intervals after vitamin A repletion, it appears that the opsin incorporated into the disc membranes of retinoid-deprived rats is able to form functi

Topics: Animals; Electroretinography; Male; Photoreceptor Cells; Pigment Epithelium of Eye; Rats; Rats, Inbred F344; Retina; Rhodopsin; Rod Cell Outer Segment; Rod Opsins; Tretinoin; Vitamin A; Vitamin A Deficiency

Dietary deficiency in the retinoid precursors of the visual pigment chromophore 11-cis-retinal eventually results in selective degeneration of the photoreceptor cells of the vertebrate retina. Early effects of retinoid deficiency are depletion of rhodopsin from the retina and vesiculation of the photoreceptor outer segment disc membranes. Experiments were conducted to determine whether these early changes were accompanied by an alteration of the opsin content of the disc membranes. After being fed a retinoid-deficient diet containing retinoic acid for 26 weeks, the rhodopsin content of rat retinas was reduced by over 85%. Both the diameters and the lengths of the outer segments decreased significantly. However, immunocytochemical and freeze-fracture analyses indicated that retinoid deficiency did not lower opsin density in the outer-segment disc membranes. These findings indicate that in the rat, opsin synthesis and disc assembly are coordinated processes that remain coupled despite reduced availability of the vitamin A chromophore. The fact that disc size decreases and disc synthesis eventually ceases in retinoid-deprived rats indicates that specific retinoids are essential for disc morphogenesis. The mechanism by which these retinoids regulate disc assembly remains to be determined.

Topics: Analysis of Variance; Animals; Diet; Freeze Fracturing; Immunoenzyme Techniques; Male; Microscopy, Fluorescence; Rats; Rats, Inbred F344; Rhodopsin; Rod Cell Outer Segment; Tretinoin; Vitamin A Deficiency

Levels of rhodopsin in the photoreceptors of Long-Evans rats were reduced by approximately 55% through dietary deprivation of vitamin A. The interaction of visual pigment with G-protein was examined in receptor outer segment (ROS) membranes obtained from these animals. A binding assay was used to quantitate affinity of the visual pigment in unbleached and bleached ROS membranes for the alpha and beta subunits of exogenous G-protein. Extents of binding were similar to those observed for ROS membranes of rats raised on a normal (vitamin A-supplemented) diet. The results are consistent with a normal capacity for G-activation by photoactivated rhodopsin (R*) in vitamin A-deprived animals. They further indicate that "free opsin" arising in vitamin A deficiency, unlike R*, has relatively low affinity for G-protein.

Topics: Animals; Electrophoresis; GTP-Binding Proteins; Heterotrimeric GTP-Binding Proteins; Light; Periodicity; Rats; Retinal Pigments; Rhodopsin; Vitamin A Deficiency

Extended vitamin A deficiency in the cat led to an abnormal appearance in the tapetal fundus with the formation of a dark brown streak centered on the area centralis. At this time rod sensitivity, as measured by the b-wave of the electroretinogram, was reduced by more than two log units; the level of rod visual pigment was reduced by about 90% throughout the paracentral retinal region and was essentially absent from the area centralis. Following oral supplementation with vitamin A there was a rapid partial recovery of both rhodopsin levels and rod sensitivity. Further recovery continued over more than 18 days to levels that were not substantially below normal. This recovery was absent from the area centralis, in which measured visual pigment levels remained very low. In supplemented cats, the brown color in the fundus faded but there remained a small hyper-reflective zone at the area centralis. Morphological examination of the central retina in a supplemented cat showed an outer nuclear layer reduced to one or two rows in the small zone with low rhodopsin levels. Cone but not rod photoreceptors were present in this zone and they appeared to lack outer segments. During recovery, the increase in rod sensitivity was approximately linearly related to the recovery of rhodopsin levels. Thus, in these conditions reduction in sensitivity resulting from previous vitamin A deficiency was limited by the ability of the photoreceptors to absorb incident quanta. The time course of the recovery of rhodopsin and sensitivity suggests that at least two processes were involved. The faster of these may be the regeneration of rhodopsin from existing opsin molecules in the outer segments, while the slower may depend on the renewal of the outer segments themselves.

Topics: Animals; Cats; Electroretinography; Fundus Oculi; Photoreceptor Cells; Retina; Retinal Pigments; Rhodopsin; Vitamin A; Vitamin A Deficiency

Details of rod and cone dysfunction in vitamin A deficiency have been studied in two subjects with primary biliary cirrhosis and one with Crohn's disease, all of whom presented with symptoms of night blindness. Visual function in the mid-peripheral retina was monitored with two-color adaptometry and rhodopsin levels were measured by fundus reflectometry. Initially all three subjects had no measurable rod function and delayed cone adaptation. In one case the dark-adapted cone threshold was also elevated. Oral supplementation with vitamin A restored visual function to normal within 8 days in all subjects. During supplementation, cone function was restored more rapidly than that of rods, though the pattern of recovery was similar for each receptor type. Final thresholds improved first, though the rates at which they were reached were abnormally slow. As recovery continued, adaptation kinetics returned to normal. When rod adaptation was delayed, the regeneration of rhodopsin was also abnormally slow. When rod final threshold was 2 log units higher than normal, rhodopsin regeneration was incomplete, reaching about 70% of the normal level. The initial stages of visual dysfunction during onset of vitamin A deficiency were studied in one subject, and were found to mirror the pattern seen during recovery: rod adaptation was initially slower than normal, but reached completion. Cone adaptation remained normal until rod function was almost absent.

Topics: Adult; Crohn Disease; Dark Adaptation; Female; Humans; Liver Cirrhosis, Biliary; Male; Middle Aged; Photoreceptor Cells; Retinal Pigments; Rhodopsin; Sensory Thresholds; Time Factors; Vision Disorders; Vision, Ocular; Visual Fields; Vitamin A; Vitamin A Deficiency

Weanling albino rats were fed a vitamin-A-adequate diet or vitamin-A-deficient diet and maintained in a cyclic light or dark environment for up to 14 weeks. One half of the rats were supplemented with additional dietary linolenic acid in the form of linseed oil. The lipid composition and rhodopsin-opsin contents of isolated rod outer segments were determined after 6-7 weeks or 12-14 weeks on diet. This study shows that feeding rats a standard vitamin A-adequate or -deficient diet results in an age-dependent loss of omega three docosahexaenoic acid and a concomitant increase in omega six docosapentanoic acid in the rod outer segments. The loss of docosahexaenoate appears to be caused by insufficient dietary omega three fatty acids. The increase in omega six docosapentanoic acid appears to arise from the high concentration of linoleic acid in standard diets containing either cottonseed, or peanut oil or supplemental corn oil. Feeding rats diets supplemented with linseed oil, however, results in a rod outer-segment lipid profile which is the same as for chow-fed animals. The same effects were seen in the fatty-acid profile of lipids from liver, although the content of polyunsaturates was much lower than in rod outer segments. Vitamin A deficiency, itself, does not lead to changes in the fatty-acid composition of either the rod outer segments or liver. After 6-7 weeks on A+ or A- diet, rhodopsin levels were, as expected, higher in dark-reared rats than in cyclic-light animals. Although the rhodopsin levels in dark-reared vitamin A-adequate rats were significantly higher than in vitamin A-deficient animals, measurements of the lipid to opsin ratio of rod outer segments indicate that the rods of vitamin A-deficient rats are not markedly different than those of vitamin A-adequate rats. It is concluded that these diets may be useful in providing a means for evaluating the role of docosahexaenoic acid in visual cell death from damaging light.

Topics: Age Factors; Animals; Docosahexaenoic Acids; Eye Proteins; Fatty Acids; Fatty Acids, Unsaturated; Linolenic Acids; Lipid Metabolism; Liver; Male; Photoreceptor Cells; Rats; Rats, Inbred Strains; Rhodopsin; Rod Cell Outer Segment; Rod Opsins; Vitamin A; Vitamin A Deficiency

Using microspectrophotometry, a study was made of the retina of adult hens, that had been kept on a diet for 6.5 months with deficiency of vitamin A. It has been shown that despite an expressed drop of quantity of vitamin A in the liver, in the external segments of the retina rods in A-avitaminosis hens, the concentration of rhodopsin remains normal.

Topics: Animals; Carotenoids; Chickens; Female; Liver; Retina; Retinal Pigments; Rhodopsin; Rod Cell Outer Segment; Spectrophotometry; Time Factors; Vitamin A; Vitamin A Deficiency

A broad-field imaging fundus reflectometer was used to determine the levels of visual pigment and their relationship to rod-mediated sensitivity in 3 patients with autosomal dominantly inherited retinitis pigmentosa. In each case the loss of sensitivity could be accounted for wholly by the decreased probability of light absorption by the rod photoreceptors resulting from the decreased levels of rhodopsin they contained. In contrast, in a subject whose night blindness was due to vitamin A deficiency, the large sensitivity loss was accompanied by a relatively small reduction in the rhodopsin level.

Topics: Female; Fundus Oculi; Humans; Ophthalmoscopes; Retinal Pigments; Retinitis Pigmentosa; Rhodopsin; Sensory Thresholds; Vision, Ocular; Vitamin A Deficiency

Topics: Animals; Diterpenes; Electroretinography; Male; Rats; Retina; Retinaldehyde; Rhodopsin; Vitamin A; Vitamin A Deficiency

Topics: Action Potentials; Animals; Dark Adaptation; Electroretinography; Male; Rats; Retina; Retinaldehyde; Rhodopsin; Stereoisomerism; Visual Cortex; Vitamin A; Vitamin A Deficiency

The levels of rhodopsin and opsin were investigated in relation to the maintenance of retinal structure in retinas of vitamin A--deficient rats in low levels of cyclic illumination (1.5 to 2 foot-candles). Rhodopsin levels decreased in the deficient retinas to approximately 20% of control at 9 weeks, and this level was retained through 39 weeks on the deficient diet. Opsin levels decreased at a slower rate but reached about 20% of control levels at 32 weeks. Despite the decrease in rhodopsin levels, obvious deterioration of disc structure was not observed until 16 weeks of deficiency, when opsin levels had already decreased to 60% to 70% of control. The structural disruption of photoreceptor outer segments was localized initially in discs of the distal third. Rod cell degeneration preceded cone cell degeneration in vitamin A--deficient retinas. Most of the rods and cones persisted in the posterior retina at 23 weeks on the deficient diet; however, by 40 weeks, only 11% of the rod nuclei remained. In contrast, about 63% of the cone nuclei were present at 40 weeks of deficiency. The photoreceptor cells were affected by the deficiency to a greater extent in the inferior hemisphere than in the superior hemisphere of the eye.

Topics: Animals; Female; Male; Photoreceptor Cells; Pregnancy; Rats; Retina; Retinal Diseases; Retinal Pigments; Rhodopsin; Vitamin A Deficiency

Most of the photoreceptors of the fly compound eye have high sensitivity in the ultraviolet (UV) as well as in the visible spectral range. This UV sensitivity arises from a photostable pigment that acts as a sensitizer for rhodopsin. Because the sensitizing pigment cannot be bleached, the classical determination of the photosensitivity spectrum from measurements of the difference spectrum of the pigment cannot be applied. We therefore used a new method to determine the photosensitivity spectra of rhodopsin and metarhodopsin in the UV spectral range. The method is based on the fact that the invertebrate visual pigment is a bistable one, in which rhodopsin and metarhodopsin are photointerconvertible. The pigment changes were measured by a fast electrical potential, called the M potential, which arises from activation of metarhodopsin. We first established the use of the M potential as a reliable measure of the visual pigment changes in the fly. We then calculated the photosensitivity spectrum of rhodopsin and metarhodopsin by using two kinds of experimentally measured spectra: the relaxation and the photoequilibrium spectra. The relaxation spectrum represents the wavelength dependence of the rate of approach of the pigment molecules to photoequilibrium. This spectrum is the weighted sum of the photosensitivity spectra of rhodopsin and metarhodopsin. The photoequilibrium spectrum measures the fraction of metarhodopsin (or rhodopsin) in photoequilibrium which is reached in the steady state for application of various wavelengths of light. By using this method we found that, although the photosensitivity spectra of rhodopsin and metarhodopsin are very different in the visible, they show strict coincidence in the UV region. This observation indicates that the photostable pigment acts as a sensitizer for both rhodopsin as well as metarhodopsin.

Topics: Animals; Diptera; Electroretinography; Light; Photoreceptor Cells; Retinal Pigments; Rhodopsin; Ultraviolet Rays; Vitamin A Deficiency

Visual pigment extracts prepared from rhabdomeric membranes of vitamin A deficient blowflies contain a 5-10 times lower concentration of rhodopsin than extracts from flies which were raised on a vitamin A rich diet. Spectrophotometry showed that digitonin-solubilized rhodopsin from blowfly photoreceptors R1-6 has an absorbance maximum at about 490 nm, but no unusually enhanced beta-band in the ultraviolet. The extracts did not contain detectable concentrations of other visual pigments nor was there any evidence for the presence of photostable vitamin A derivatives. Sodium dodecyl sulfate polyacrylamide gel electrophoresis demonstrated that the concentration of opsin in the rhabdomeric membrane is significantly reduced in vitamin A deficient flies compared to normal flies. The results indicate that the synthesis of opsin or its incorporation into the photoreceptor membrane is regulated by the chromophore concentration in the receptor cell. Furthermore, our findings open up the possibility that differences in the spectral absorption and excitability of photoreceptors from normal and vitamin A deficient flies result from the differing opsin content of the rhabdomeres.

Topics: Animals; Cell Membrane; Diptera; Photoreceptor Cells; Retinal Pigments; Rhodopsin; Spectrophotometry; Vitamin A Deficiency

Topics: Animals; Drosophila melanogaster; Electroretinography; Light; Membrane Potentials; Mutation; Photoreceptor Cells; Rhodopsin; Spectrum Analysis; Vitamin A Deficiency

Rhodopsin kinetics and visual threshold were determined in three subjects with a dominant form of retinitis pigmentosa. The retinal areas studied showed varying loss of sensitivity, which correlated well with the reduction in the measured density of rhodopsin in the test region. Rhodopsin photosensitivity was normal, and there was no evidence that either rhodopsin or the cone pigments regenerated more rapidly than normal. The findings in these cases of retinitis pigmentosa, when compared with the threshold changes induced by vitamin A deficiency or photic bleaching, suggest that the disease produces an imbalance between disc removal and new disc formation, which results in a progressive shortening of the photoreceptor outer segments and, eventually, in their complete disappearance.

Topics: Adult; Female; Humans; Light; Male; Middle Aged; Ophthalmology; Retina; Retinal Pigments; Retinitis Pigmentosa; Rhodopsin; Visual Acuity; Vitamin A Deficiency

Topics: Animals; Drosophila melanogaster; Electroretinography; Freeze Fracturing; Microscopy, Electron; Photoreceptor Cells; Retinal Pigments; Rhodopsin; Vitamin A Deficiency

Topics: Animals; Behavior, Animal; Male; Rats; Retina; Retinal Pigments; Reward; Rhodopsin; Time Factors; Vision, Ocular; Vitamin A Deficiency

Many photoreceptor cells in invertebrates have a dual-peak spectral sensitivity. Evidence is presented that in fly photoreceptors the ultraviolet peak is due to a photostable pigment that absorbs light quanta and transfers the energy to the blue-absorbing visual pigment.

Topics: Animals; Diptera; Energy Transfer; Models, Biological; Photoreceptor Cells; Retinal Pigments; Rhodopsin; Spectrophotometry, Ultraviolet; Vision, Ocular; Vitamin A Deficiency

Topics: Age Factors; Animals; Darkness; Diet; Light; Pigment Epithelium of Eye; Rats; Retina; Retinal Degeneration; Retinal Pigments; Rhodopsin; Time Factors; Vitamin A; Vitamin A Deficiency

Topics: Acetates; Administration, Oral; Animals; Body Weight; Dose-Response Relationship, Drug; Electroretinography; Injections, Intraperitoneal; Isomerism; Male; Night Blindness; Organ Specificity; Rats; Retina; Rhodopsin; Testis; Vitamin A; Vitamin A Deficiency