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[Histopathologic and immunohistochemical studies on retina after laser photocoagulation].

OBJECTIVE: To observe the histopathologic and immunohistochemical changes and reparable process of retina after laser photocoagulation in order to provide a theoretical basis of laser treatment for fudus diseases. METHODS: Normal retina was photocoagulated using I-, II-, III-grade photic spot after the signing of informed consent of 7 patients who were suffering from orbital malignant tumors and in need of exenteration. The retinae from removed eyeballs were fixed with formalin, imbedded in paraffin and stained by H. E. The SP immunohistochemical method was adopted using antibodies of S-100, GFAP, NSE,and NF label. RESULTS: By histopathologyical examination, 1 day after photocoagulation with I-grade photic spot, the retinal pigment epithelium (RPE) cells, photoreceptors and cells in outer nuclear layer were edematous and necrotic, and decreased in number; with II-grade photic spot, many RPE cells, photoreceptors and cells in outer nuclear layer were lysed and destroyed; with III-grade photic spot, all layers of the retina were severely damaged. 3 days after photocoagulation, retinal edema was relieved. RPE and glial cells started proliferating. 7 days after photocoagulation, RPE and glial cells proliferated obviously to cover the destroyed areas. By immunohistochemistry, 3-7 days after photocoagulation, S-100 and GFAP were seen stained in the damage areas of photic spot. 1-7 days after photocoagulation, NSE and NF were found unstained in the photic spot. CONCLUSION: The above data indicated that different laser photic spots resulted in various degrees of damage to the retina. The destroyed regions were repaired by proliferative RPE and glial cells. Immunohistochemistry confirmed that proliferative gial cells repaired damaged retina, and neurons and nerve fibers could not regenerate. Laser could treat different retinal diseases.

Glial Fibrillary Acidic Protein↗

[Protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia and reperfusion-injury of rat retina].

OBJECTIVE: To study the protective effect of electrical stimulating cerebellar fastigial nucleus on ischemia-reperfusion-injury of rat retina. METHODS: Rats were divided randomly into group of ischemia-reperfusion, group of electrical-stimulation-treated and group of sham-operated. The duration ischemia was 1 hour except sham-operated. In treated group, harvests of retinas followed electrical stimulation of cerebellar fastigial nucleus for 60 min after reperfusion for 6 hours; in reperfusion group, retinas were harvested only after 6 hours reperfusion. Retinal ischemia was produced in rats by ligating vessels and the optic nerve for 1 hour. Expression of inducible nitric oxide synthase (iNOS) in retina was measured by NADPH-NDP histochemistry; Apoptosis was measured by Tdt-dUTP terminal nick-end labeling (TUNEL) method. Morphology change was observed with the help of HPIAS-1000 auto-medical-imagined computer analyzer. RESULTS: (1) The thickness of inner retinal (including outer plexiform layer, inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrane) and the inner plexiform layer were increased significantly in ischemia-reperfusion group than those in treated group. (2) The morphological changes of the scattered and condensed nucleus were observed more slightly under light microscopy in treated group than those in ischemia-reperfusion group. (3) Expression of inducible nitric oxide synthase (iNOS) in retinal ganglion cell in treated group is more significant than in ischemia-reperfusion group. (4) The amount of apoptosis cells in retina in treated group is significantly less than thatin ischemia-reperfusion group. CONCLUSIONS: (1) The results indicated that ischemia-reperfusion injury can induce retinal apoptosis. Retinal apoptosis can be inhibited by electrical stimulation cerebellar fastigial nucleus. (2) iNOS maybe involved in the mechanism of apoptosis. (3) Cerebellar fastigial nucleus electrical stimulation can protect ischemia-reperfused retina.

Animals↗

[Effects of extracts of ginkgo biloba (EGB) on levels of nitric oxide and apoptosis in the retina induced by glutamate in adult rabbits].

OBJECTIVE: To study the effects of extracts of ginkgo biloba (EGB) on the levels of nitric oxide (NO) and apoptosis in the retina induced by glutamate by intravitreal injection in adult rabbit. METHOD: The model of apoptosis in retina induced by glutamate by intravitreal injection was established in adult rabbit and EGB was retrobulbarly injected. The levels of NO were measured by spectrophotometer. Retina DNA fragmentation was determined by agarose gel electrophoresis. RESULT: The levels of NO in retina in experiment groups were significantly increased compared with controls, after treatment with high dosage of EGB, and levels of NO was decreased to normal. They were not decreased by injection of small dosage of EGB. DNA fragmentation of retina apoptosis was detected in experiment groups and small dosage EGB groups. CONCLUSION: The retina apoptosis was induced by glutamate by intravitreal injection in adult rabbit and was inhibited by EGB that may be through blocking the generation of NO free radicals.

Animals↗

Differential regulation of melatonin synthesis genes and phototransduction genes in embryonic chicken retina and cultured retinal precursor cells.

PURPOSE: Photoreceptor differentiation involves the activation of two specific sets of genes; those encoding the proteins of the phototransduction cascade and those encoding the enzymes of the melatonin synthesis pathway, arylalkylamine N-acetyltransferase (AANAT) and hydroxyindole O-methyltransferase (HIOMT). The purpose of the present study was to examine the conditions of AANAT and HIOMT gene activation, relative to that of selected phototransduction markers (alpha-transducin and opsins), in both in vivo and in vitro differentiating photoreceptors of the chicken retina. METHODS: Neural retina RNA was obtained between embryonic day 7 (E7) and posthatch day 8 (P8) and analyzed on northern blots with cDNA probes to AANAT, HIOMT, visinin, alpha-transducin, rhodopsin, and the four cone opsins. Cell cultures were prepared from E7 chicken neural retina and incubated for two to four days in vitro, either in basal medium or in serum-supplemented medium or in medium containing an insulin-based supplement. RNA from the cultured cells was analyzed on northern blots as above. Real time RT-PCR was used to confirm in vitro changes in HIOMT and red opsin mRNA levels. The cultured cells were transfected with promoter-reporter plasmids for direct analysis of HIOMT promoter regulation by the dual luciferase method. RESULTS: The different mRNAs composing the photoreceptor phenotype appeared at E7 (visinin), E10 (alpha-transducin), E14 (HIOMT), E15 (rhodopsin, red opsin, and green opsin), E16 (AANAT), E17 (blue opsin), and E18 (violet opsin). In the early differentiating cones of the central retina, HIOMT mRNA appeared two days earlier than red opsin and green opsin mRNAs (E12 rather than E14). In cultured embryonic neural retina cells, basal medium was sufficient to activate alpha-transducin gene transcription, an insulin-based supplement was sufficient to activate HIOMT gene transcription, whereas serum was required for red opsin gene transcription after two days in vitro. All serum batches were able to activate red opsin gene transcription, whereas some of them failed to activate HIOMT gene transcription. Activation of the HIOMT gene promoter by an insulin-based supplement and by serum was confirmed after transfection of chicken embryonic neural retina cells with promoter-reporter plasmids. CONCLUSIONS: Activation of the melatonin synthesis genes in vivo takes place in a time window very close to that of early opsins. However, a 24-48 h lead of HIOMT gene expression over early opsins was clearly observed. Our in vitro experiments indicate that different exogenous signals are required to activate the different genes encoding photoreceptor specific functions. Significantly, marker genes for light sensitivity (red opsin) and for melatonin synthesis (HIOMT) appear to be activated in response to different signals.

Acetylserotonin O-Methyltransferase↗

Radioautographic study on DNA synthesis of the retina and retinal pigment epithelium of developing mouse embryos.

We report the changes of proliferative activity of the retina and retinal pigment epithelium (RPE) of mouse embryos by detecting cells in the S-phase by light microscopic radioautography using 3H-thymidine. The eyes germs of mouse embryos at the embryonic days 9.5 (E 9.5), E 11.5, E 13.0, E 15.5, E 18.5 of gestational ages, were used for this experiment. Small pieces of the ocular tissues were labelled with 3H-TDR in vitro and light microscopic radioautographs were prepared. The labeling indices of the respective regions of tissues were calculated. Both tissues of retina and RPE showed high percentages of labeling indices from 10% to 50% through the developmental stages. The labeling indices of both tissues in earlier stages were generally higher than those of later stages, and gradually decreased in the later stages. However, the retina and RPE showed different courses of the changes of labeling indices respectively during the embryonic development. In the retina, the labeling indices in the vitreal portions were more than those in the scleral portions during the earlier developmental stages. However, in the later stages, the indices of scleral portions were more than those in the vitreal portions. Comparing the three regions of retina, the labeling indices of the anterior regions were generally higher than those of the equatorial and posterior regions, especially in the vitreal portion. Remarkable differences among three regions were not found in the scleral portion. In the RPE, the labeling indices gradually increased in the anterior region, but decreased in the equatorial and the posterior regions through all the developmental stages. The proliferation of both retina and RPE in the central region occurred earlier than those of the peripheral region.

Animals↗

[Morphological changes of retina after N-methyl-D-aspartate induced damage in rats].

OBJECTIVE: To investigate N-methyl-D-aspartate (NMDA)-induced morphological changes in the retina in rats. METHODS: Thirty-two healthy Sprague-Dawley (SD) rats were randomly divided into 4 groups. Eight rats were in normal control group. The rest 24 rats were equally distributed into 3 experimental groups to receive a single dose of 2 microL intravitreal injection of 3 different concentrations of NMDA (namely 10 nmol, 20 nmol, and 40 nmol per injection ) into the right eyes. The left eyes received 2 microl 0.1 mol PBS used as a self-control. Seven days after the NMDA injection, all rats were killed and the eyes were enucleated. The extent of NMDA-induced neurotoxicity in the retina was quantified by the thickness of the inner plexiform layer (IPL) of the retina at 1.0 - 1.5 mm from the margin of the optic disc of 6 rats in each group. The retinas and optic nerves from the other 2 rats were processed for histopathologic investigation under electronic microscope and light microscope. RESULTS: The thickness of IPL was decreased. There was significant difference between any of the above 2 groups (All P < 0.05). The higher the concentration of NMDA solution, the more decreased thickness of the IPL. No obvious abnormality was observed in the outer layer of the retina. There was degeneration of the optic nerve axons in the NMDA-treated eyes of the experimental groups. The extent of morphological changes of the axons of the optic nerve was related to the dose of NMDA administrated. Ultra-structural study also showed some characteristic changes of apoptosis such as shrunken nucleus and clumping of chromatin at the nuclear membrane in retinal ganglion cell lay (RGCL) and inner nuclear layer (INL). CONCLUSION: Administration of NMDA can result in the thinning of IPL and the dose-dependent degeneration of the optic nerve. Apoptosis may be the main morphological evidence of NMDA receptor-mediated cell death in RGCL and INL in adult rat retinas. NMDA-induced damage is similar to glaucomatous degeneration to some extent.

Animals↗

[The changes of histology and biochemical parameters in retina of the patient with diabetic retinopathy].

OBJECTIVE: To observe and estimate the distribution the changes of histology and biochemical parameters in retina of the patient with diabetic retinopathy. METHODS: Retinas were divided into quadrants and the lesions of diabetic retinopathy were compared among quadrants. the vasculature was isolated by trypsin-digest, homogenates taken from temporal and nasal quadrant were used to explore regional differences in the expression of Glut-1, PKCbeta and activity of caspase1. RESULTS: Microaneurysms, acellular capillaries and pericytes ghosts were significantly increased in the temporal retina than in the nasal retina. Activity of the pro-inflammatory protease, caspase1, was the only biochemical abnormality which was found significantly difference between quadrants. Glut-1 expression was decreased in diabetes, but there was no significant difference between quadrants. Expression of PKCbeta in both temporal and nasal retina was tended to be greater in diabetic than in non diabetic patients. CONCLUSION: Retinal microvascular disease does not develop uniformly across the retina, even the different regions are exposed to the same level of hyperglycemia. Regional differences play an important role in the response of the retinal microvasculature to hyperglycemia.

Aged↗

Gene expression profiles of intact and regenerating zebrafish retina.

PURPOSE: Investigate the molecular determinants of retinal regeneration in adult vertebrates by analyzing the gene expression of control and post-lesion retina of adult zebrafish, a system that regenerates following injury. METHODS: Gene expression of zebrafish retina and brain were determined with DNA microarray, RT-PCR, and real-time quantitative PCR analyses. Damaged retinas and their corresponding controls were analyzed 2-5 days post-lesion (acute injury condition) or 14 d post-lesion (cell regeneration condition). RESULTS: Expected similarities and differences in the gene expression profile of zebrafish retina and brain were observed, confirming the applicability of the gene expression techniques. Mechanical lesion of retina triggered significant, time-dependent changes in retinal gene expression. The induced transcriptional changes were consistent with cellular phenomena known to occur, in a time-dependent manner, subsequent to retinal lesion, including cell cycle progression, axonal regeneration, and regenerative cytogenesis. CONCLUSIONS: The results indicate that retinal regeneration in adult zebrafish involves a complex set of induced, targeted changes in gene transcription, and suggest that these molecular changes underlie the ability of the adult vertebrate retina to regenerate.

Animals↗

Induction of vitronectin and integrin alphav in the retina after optic nerve injury.

PURPOSE: Vitronectin is a secreted glycoprotein present in blood plasma and is present in the extracellular matrix of many tissues. It was found in the retinal cDNA library that contains genes whose expression is upregulated after optic nerve injury in a previous study. The purpose of this study was to assess the temporal and spatial changes in expression of vitronectin and integrin alphav in the retina following optic nerve injury. METHODS: Adult Balb/c mice underwent crush of the optic nerve in one eye only. RT-PCR was used to determine the temporal expression of vitronectin mRNA in the retina after injury. In addition, expression at the protein level in the retina and the optic nerve of vitronectin and its major receptor subunit, integrin alphav, was analyzed by immunohistochemistry. RESULTS: Upregulation of vitronectin mRNA in the retina was detected at one day after injury, peaking at three days, and maintained up to one week. An elevated expression of vitronectin protein was also observed in the inner retina, optic nerve head, and the optic nerve after nerve crush. In the inner retina, the increased expression of vitronectin was found in retinal ganglion cells (RGCs) and its surrounding extracellular matrix. Expression of integrin alphav was also increased in the RGC layer and in the glial cells of the nerve head and the crush site. CONCLUSIONS: As vitronectin is an extracellular protein that can support cell attachment and promote neurite extension, elevated expression of vitronectin and its receptor may facilitate axonal regeneration following injury. We propose that treatment sustaining secretion of endogenous vitronectin or direct application of exogenous vitronectin may be a method to augment regeneration of the severed optic axons.

Animals↗

Effects of induced systemic hypothyroidism upon the retina: regulation of thyroid hormone receptor alpha and photoreceptor production.

PURPOSE: Investigate the effects of systemic hypothyroidism upon the differentiated, growing, and regenerating retina of postmetamorphic winter flounder, a vertebrate that experiences a thyroid hormone (TH) induced metamorphosis during development. METHODS: A loss-of-signal strategy was utilized in which TH signaling was disrupted by inhibiting TH synthesis. Induced hypothyroidism was confirmed by radioimmunoassay. Reverse transcriptase PCR (RT-PCR), real-time quantitative PCR (qPCR), molecular cloning, non-isotopic in situ hybridization, western blot analysis, and indirect immunohistochemistry techniques were performed to analyze retinal thyroid hormone receptors (TR), photoreceptor production, and the phenotypic repertoire of differentiated retinal cells as a function of TH signaling status. RESULTS: Molecular bases for TH signaling were supported by retinal expression of TH receptors alpha and beta. TH-dependent transcriptional regulation of TRalpha but not TRbeta was indicated, with induced hypothyroidism producing an increase in TRalpha expression. Evidence for post-transcriptional regulation of retinal TRalpha was observed. The repertoire of inner retinal cell types in premetamorphic fish (a naturally low TH condition) matched that observed in the central retinas of both normal postmetamorphic fish (a naturally elevated TH condition) and postmetamorphic fish rendered hypothyroidic. In differentiated postmetamorphic retina there was no evidence for significant differences in opsin expression between normal and hypothyroidic animals. Induced hypothyroidism did, however, significantly affect the types of photoreceptors that were produced in postmetamorphic retina: as a hypothyroidic postmetamorphic retina grew or regenerated following injury, the phenotypic repertoire of newly-produced photoreceptors matched that observed for premetamorphic retina, in which rods, SWS2-expressing "blue" cones, and LWS-expressing "red" cones are absent, and only the RH2-expressing "green" cone type is present. The effects of induced hypothyroidism upon photoreceptor specification (manifestation of the rod lineage) and differentiation (expression of a particular opsin by specified cones) were apparently reversible. CONCLUSIONS: The results suggest a TH-dependent regulation of retinal TRalpha, a lack of TH-dependent regulation of the phenotypic identity of differentiated retinal cells, and the operation of similar cytogenic mechanisms during retinal growth and regeneration. The principal conclusion is that TH signaling significantly affects, in a targeted manner, the production of both rod and cone photoreceptors during retinal growth and regeneration.

Animals↗

Immunohistochemical localization of substance P, enkephalin and serotonin in the developing human retina.

The localization of substance P (SP), enkephalin (ENK) and serotonin (5-HT) in the retinae of 12 human embryos/fetuses ranging in age from 6-30 weeks was determined immunohistochemically using the PAP method. At the 6 week stage [crown rump length (CRL) unknown due to incomplete specimen], the developing retina consisted of a single undifferentiated cell mass from which immunoreactive cells were absent. By 90 mm CRL (10th week of gestation), the retina was composed of an outer neuroblastic layer, an inner plexiform layer and an innermost layer of ganglion cells. At this stage, SP, ENK and 5-HT positive cells were detected solely in the outer neuroblastic layer. By 140 mm CRL (17 weeks), the retina consisted of cell layers similar in number and type to those of the adult retina. In specimens 140-216 mm CRL (gestation ages 17-24 weeks), SP, ENK and 5-HT neurons were present in the outer nuclear, inner nuclear and inner plexiform layers. In addition, 5-HT positive neurons and fibers were evident in the outer plexiform layer. By 285-295 mm CRL (26-30 weeks), neurons in the ganglion cell layer and the fovea were also SP and ENK positive. In earlier specimens, the cell bodies alone were immunopositive and not until 142 mm CRL (17 weeks) were positive processes observed. Finally, the presence of SP, ENK and 5-HT immunopositive structures occurred in a sequence from outer to inner layers of the developing human retina.

Embryo, Mammalian↗

Effect of accelerated iron ions on the retina.

The eyes of rats were exposed to doses of 0.1 and 2.5 Gy of 450-MeV/amu 56Fe particles (LET approximately 195 keV/microns). The beam axes were oriented perpendicular to the central retina of the animals. Retinas were harvested immediately (less than 10 min), 24 h, 15 days, 136 days, and 186 days after the experiment. The retinas of animals of equivalent ages were sampled at the same intervals. By Day 15, the spatial densities of the pigment epithelial, photoreceptor, and bipolar cells in retinas irradiated with 2.5 Gy were 15 to 20% lower than those of the controls. The cellular density of the pigment epithelium returned to the control level by Day 186 while photoreceptor and bipolar cell numbers remained depressed. One and fifteen days after irradiation, the choroidal vessels showed signs of radiation damage. Exposure to 0.1 Gy did not affect the cellular density within the retina at the interval examined (186 days). None of the retinas showed evidence of track-specific injury that could be interpreted as microlesions or tunnel lesions.

Animals↗

[Protein inhibitor of cyclic nucleotide phosphodiesterase in the retina in hereditary degeneration].

Thermostable protein fraction from retina of rats with hereditary retinal dystrophy (Hunter and Campbell strains) did not inhibit cyclic nucleotide phosphodiesterase. At the same time an inhibitory component, found in retina of Wistar rat, rabbit, frog and lamprey, was similar to the component from bovine retina. Quantity of the inhibitory component in normal rat retina decreased considerably within postnatal period (12 days--3 months). Thermostable proteins, isolated from Campbell rat retina, differed from that of Hunters' one by electrophoretic properties while both preparations were dissimilar to the protein of normal rat. Protein bands, containing inhibitory component from dystrophic rat retina, appear to be less distinct as compared to those of normal rat. These proteins, eluated from the bands of Campbell rats, activated phosphodiesterase but the preparations from Hunter rats did not influence on it.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

Oxygen distribution and consumption in the cat retina at increased intraocular pressure.

Oxygen microelectrodes were used to study the distribution of oxygen in the retina of dark adapted anesthetized cats during short term elevation of intraocular pressure (IOP) that reduced the perfusion pressure (PP = mean femoral arterial pressure - IOP) to as low as 40 mm Hg. The oxygen tension (PO2) in the inner half of the retina was affected very little over this range. Choroidal PO2, however, decreased substantially, about 0.5 mm Hg per mm Hg perfusion pressure, in the area centralis and superior retina (15-20 degrees superior to the area centralis). This decreased the oxygen available to that part of the outer retina supplied by the choroidal circulation. Oxygen consumption was estimated by fitting profiles of PO2 as a function of distance to a diffusion model. This analysis showed that photoreceptor oxygen consumption decreased significantly at perfusion pressures less than 70 mm Hg in the area centralis. Changes in consumption were also observed in the superior retina, but were not significant. Oxygenation of a region just nasal to the optic disc was also studied, but neither the choroidal PO2 nor oxygen consumption in this area was affected over the range of PP studied. These results provide direct evidence that moderately increased IOP leads to a decrease in choroidal PO2 and sufficient hypoxia in the distal retina to cause a reduction in photoreceptor oxygen consumption. This presumably slows the photoreceptor Na+/K+ pump and leads to the ERG changes reported previously (Yancey and Linsenmeier, Invest Ophthalmol Vis Sci 29:700, 1988).

Animals↗

Effects of hyperoxia on the oxygen distribution in the intact cat retina.

Double-barreled oxygen microelectrodes were used to measure the distribution of oxygen within the dark adapted cat retina during systemic hyperoxia (100% O2 inspired). Oxygen tension (PO2) decreased monotonically from the choroid to the vitreous humor in most cases, showing that a greater portion of the retina was supplied by the choroid during hyperoxia than during normoxia. In the proximal half of the retina the PO2 increased during hyperoxia by an average of about 40 mm Hg, while the increase in the distal retina was larger. At the choroid the average increase in PO2 was about 150 mm Hg. Analysis of the oxygen profiles showed that photoreceptor oxygen consumption was unchanged during hyperoxia. Retinal PO2 increased rapidly at the beginning of hyperoxia, and often partially recovered from its peak value during hyperoxia, even in the distal retina, suggesting that the choroidal circulation may have some limited autoregulatory capacity. As in normoxia, retinal illumination led to an increase in PO2 in the distal retina, due to a decrease in oxygen consumption. The light-evoked increase in PO2 was larger during hyperoxia, but the underlying change in oxygen consumption was probably the same as in normoxia.

Animals↗

Acetylcholine receptors in the human retina.

Evidence for a population of acetylcholine (ACh) receptors in the human retina is presented. The authors have used the irreversible ligand 3H-propylbenzilylcholine mustard (3H-PrBCM) to label muscarinic receptors. 3H- or 125I-alpha-bungarotoxin (alpha-BTx) was used to label putative nicotinic receptors. Muscarinic receptors are apparently present in the inner plexiform layer of the retina. Autoradiographic grain densities are reduced in the presence of saturating concentrations of atropine, quinuclidinyl benzilate or scopolamine; this indicates that 3H-PrBCM binding is specific for a population of muscarinic receptors in the human retina. Binding sites for radiolabeled alpha-BTx are found predominantly in the inner plexiform layer of the retina. Grain densities are reduced in the presence of d-tubocurarine, indicating that alpha-BTx may bind to a pharmacologically relevant nicotinic ACh receptor. The work reported here is consistent with earlier data on cholinergic neurons in the retina of other mammalian species, as well as with previous work on the psychophysical effects of cholinergic agonists on human vision. This study provides evidence for cholinergic neurotransmission in the human retina.

Acetylcholinesterase↗

Regional distribution of glutathione peroxidase and Glutathione-S-transferase in adult and premature human retinas.

The activities of glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GSH-S-tase) were investigated in adult and premature human retinas. The measurements were done in the vascular and avascular regions of premature retinas at gestational age of 22-33 weeks and in the central, mid-peripheral, and far peripheral regions of mature retinas from the age of 1 month to 73 years. Among the premature infants, those who survived for greater than 24 hours were supplemented with alpha-tocopherol (vitamin E) on a periodic basis. The vascular and avascular regions of premature retinas had higher activities of GSH-Px when compared to the central and far peripheral regions of mature retinas. Infants surviving more than 24 hr had higher activities of GSH-S-tase in the avascular region than infants who survived less than 24 hr. Survival did not affect either enzyme activity in the vascular regions. Mature retinas showed a decrease in GSH-Px specific activity with age, but no age-related changes in GSH-S-tase were observed. These data demonstrate that premature infants are born with relatively high levels of GSH-Px and GSH-S-tase.

Adolescent↗

Carotenoids in the human macula and whole retina.

The carotenoid pigments in the whole human retina and in the macular region were measured quantitatively by high pressure liquid chromatography (HPLC). Approximately a five-fold larger amount of carotenoids was found in the human macula (35-120 ng) than in previously reported work. The dominant carotenoids in the whole retina are lutein and zeaxanthin. Zeaxanthin is concentrated in the macular region, whereas lutein is dispersed throughout the entire retina. Contrary to prior reports, substantial quantities of both carotenoids are present in the infant retina. Increasing variability is observed in carotenoid levels between individuals with advancing age, and some older individuals show very high whole retina carotenoid levels. These quantitative studies were made possible by synthesis of a new, stable carotenoid internal standard. Carotenoids have been proposed to be potent antioxidants, protecting membrane lipids from toxic peroxidation reactions. The method presented in this study will facilitate quantitative investigations of the association between carotenoid levels and health and disease of the retina.

Aging↗