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E Zemel

Publications and source records attributed to E Zemel.

14 recordsLinked to original sources
PubMed2002

Early retinal damage in experimental diabetes: electroretinographical and morphological observations.

A growing body of evidence indicates that impairment of retinal function precedes the earliest signs of vascular complications. The aim of this study was to follow the development of retinopathy both functionally and morphologically in a rat model of diabetes mellitus. Diabetes was induced in rats by intravenous injection of streptozotocin (STZ). Age-matched rats raised under similar conditions served as control. The electroretinogram (ERG) was recorded in order to assess retinal function. The expression of glial fibrillary acidic protein (GFAP) in Müller cells was used as a cellular marker for retinal damage. The ERG responses of the diabetic rats were reduced in amplitude compared to the responses recorded from the control rats as early as 2 weeks after onset of diabetes. The b-wave was more affected than the a-wave. GFAP expression in the diabetic retina did not differ from that in the control retina during the first 5 weeks of diabetes. GFAP was demonstrated only in astrocytes in the vitreo-retinal border. After 6-7 weeks of diabetes, GFAP expression in the retinas of the diabetic rats was also detected in the endfeet of the Müller cells. With the progression of diabetes, GFAP expression spreads throughout the entire length of the Müller cells. In the retinas from control rats, GFAP expression was limited to astrocytes and was not detected in Müller cells even at 40 weeks of follow-up. The observations indicate that the functional integrity of retinal cells is compromised already at short time intervals after onset of experimental diabetes in rats.

Animals↗
PubMed2001

NADPH diaphorase activity in the rabbit retina is modulated by glutamatergic pathways.

NADPH diaphorase activity in the rabbit retina is modulated by the state of visual adaptation. In this study, we tested possible glutamatergic control of this phenomenon. Rabbits were injected intravitreally with agonists and antagonists of glutamate. After adaptation (3 hours) to either room light or darkness, the rabbits were killed and the retinae were prepared for NADPH diaphorase histochemistry. Kainic acid significantly reduced the number of NADPH diaphorase amacrine cells but augmented NADPH diaphorase activity in horizontal cells in both light- and dark-adapted animals. 6,7-Dinitroquinoxaline-2,3(1H,4H)-dione exerted no effect on amacrine cells but eliminated NADPH diaphorase activity in horizontal cells. 2-Amino-4-phosphono butyric acid did not affect NADPH diaphorase activity in horizontal cells but reduced the degree of staining in the neuronal processes of amacrine cells. MK-801 and N-methyl-D-aspartic acid (NMDA) had no effect on NADPH diaphorase activity in horizontal cells. However, MK-801 reduced staining in the neuronal processes of amacrine cells but not in their cell bodies. NMDA effects were expressed in a significant reduction in the number and size of amacrine cells that were NADPH diaphorase positive. These results indicate that activation of NADPH diaphorase in horizontal cells by darkness is mediated by the activation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainic acid (KA)-type glutamate receptors. The ON pathway in the retina is probably involved in modulation of NADPH diaphorase in the neuronal processes of amacrine cells. Amacrine cells that are NADPH diaphorase positive contain NMDA-type and AMPA/KA-type receptors and are highly susceptible to NMDA and kainic acid toxicity.

Adaptation, Ocular↗
PubMed2001

Retinal toxicity of gentamicin after subconjunctival injection performed adjacent to thinned sclera.

OBJECTIVE: To investigate the potential toxicity to the retina of gentamicin injected near surgically thinned scleral areas in a rabbit model. DESIGN: Experimental study. METHODS: Scleral scraping to half thickness was performed in the superotemporal scleral area in both eyes of adult rabbits (n = 10). Gentamicin sulfate was injected subconjunctivally to the right eye and saline to the left eye, which always served as a control eye. Four weeks after the procedure, electroretinography (ERG) was performed to assess retinal function. Then, the eyes were enucleated and prepared for histologic evaluation of structural damage. In four eyes of two additional rabbits, vitreous gentamicin concentrations were measured using a fluorescence polarization assay. MAIN OUTCOME MEASURES: Dark- and light-adapted ERG responses and histopathologic damage. RESULTS: Dark- and light-adapted ERG responses in all rabbits were similar in the experimental and control eyes. Gentamicin levels were more than 10 microg/ml after subconjunctival injection of gentamicin with scraping and 0.29 microg/ml after subconjunctival injection of gentamicin with no scraping. Histopathologic examination revealed significant local damage to the photoreceptors adjacent to the area of scraping and subconjunctival injection. A significantly lesser degree of damage was seen if gentamicin was injected in pigmented rabbits or in albino rabbits, but only 4 weeks after scleral scraping. CONCLUSIONS: Increased penetration of gentamicin through thinned sclera may lead to toxic levels of the drug in a localized area adjacent to the site of injection. These toxic effects are also influenced by the degree of pigmentation and acute inflammation.

Animals↗
PubMed1999

Development of laser-induced retinal damage in the rabbit.

BACKGROUND: Laser lesions may induce retinal damage that is larger than expected from the size of the coagulated area. This study was designed to follow the development of laser-induced reduction in retinal function and to correlate it with structural changes. METHODS: Pigmented rabbits were treated in one eye with 225 argon laser lesions. The ERG responses were recorded at different times after treatment. The effect of the laser treatment upon the functional integrity of the retina was assessed from the ERG responses. Structural damage was examined by light microscopy. RESULTS: Shortly (1-2 h) after laser treatment, the ERG responses were reduced by about 50%. ERG deficit continued to develop and reached a maximal level about 24 h after treatment. Thereafter, slow recovery was observed but permanent deficit, relative to the initial laser effect, was seen even 30 days after treatment. Histological observations indicated extensive serous retinal detachment between laser lesions that developed within 24 h after treatment. At 30 days post-treatment, lesioned areas were completely destroyed and heavily pigmented. The retina between lesions was attached to the pigment epithelium but exhibited different degrees of structural damage. CONCLUSIONS: The immediate laser damage is confined to the coagulated areas while secondary functional damage develops within 24 h and probably reflects serous retinal detachment between lesions. The serous retinal detachment completely resolves with time but may induce permanent structural abnormalities in non-coagulated retinal areas that is reflected in a functional deficit larger than the initial laser effect.

Animals↗
PubMed1995

The effects of lidocaine and bupivacaine on the rabbit retina.

The toxic action of two commercial anesthetics, lidocaine and bupivacaine, on the functional and morphologic integrity of the retina was investigated in albino and pigmented rabbits. The experimental drug was injected into the vitreous of one eye, while saline solution was injected into the fellow eye. Retinal function was assessed from the electroretinogram and the visual evoked potential. Retinal structure was examined at the light microscopic level. Ten milligrams of lidocaine did not affect the electroretinogram and the visual evoked potential responses, though structural damage could be detected close to the site of injection. A lower dose of 5 mg did not produce any detectable physiologic or morphologic damage. The only dose of bupivacaine used, 0.5 mg, was not toxic to the albino and pigmented rabbit retinas, as assessed by the electroretinogram, visual evoked potential, and light microscopy. The results of this study demonstrate that lidocaine and bupivacaine are nontoxic to the rabbit retina at concentrations that are effective for retrobulbar anesthesia.

Anesthetics, Local↗
PubMed1995

Ocular pigmentation protects the rabbit retina from gentamicin-induced toxicity.

PURPOSE: This study was designed to investigate the possibility that gentamicin-induced retinal toxicity is dependent on ocular pigmentation by comparing the effects of the drug on the functional and morphologic integrity of the retina in albino and pigmented rabbits. METHODS: In each rabbit, a solution of gentamicin sulfate was injected into the vitreous of one eye, and saline was injected into the other eye. Retinal function was assessed by electroretinogram (ERG) at different time intervals after injection. Retinal structure was examined at the light microscopic level. RESULTS: In albino and pigmented rabbits, functional retinal damage developed to a maximal level within the first week after gentamicin injection. Thereafter, gradual recovery could be seen in eyes that suffered less than 80% maximal reduction in the ERG b-wave. For each dose >0.1 mg studied, retinal damage was more severe in the albino rabbits than in the pigmented ones. The degree of damage was not affected by the level of ambient illumination, nor was it reduced by the administration of N-acetylcystein, a free radical scavenger, together with gentamicin. CONCLUSIONS: Ocular pigmentation partially protects the rabbit retina from the toxic action of gentamicin. This protection probably reflects binding of the drug by the melanin, which thereby reduces the concentration of the free gentamicin. When the initial gentamicin-induced retinal damage is expressed in < 80% reduction in the ERG, substantial recovery may occur in both strains of rabbits.

Albinism↗
PubMed1993

Drug-induced retinal toxicity in albino rabbits: the effects of imipenem and aztreonam.

PURPOSE: To test the toxic action of two antibiotics, imipenem and aztreonam, on the functional and morphologic integrity of the albino rabbit retina. METHODS: Two commercial drugs were used--Tienam, which contains imipenem, and Azactam, which contains aztreonam. Different doses of these drugs were injected intravitreally. Retinal function was assessed from the electroretinogram (ERG) and the visual evoked potential (VEP). Retinal structure was examined at the light microscopic level. RESULTS: Imipenem did not affect the ERG and the VEP responses or the morphology of the retina up to a total injected dose of 0.98 mg (2 mg Tienam). Aztreonam was not toxic to the albino rabbit retina up to a total injected dose of 2.8 mg (5 mg of Azactam). Severe functional and morphologic retinal damage was seen when 10 mg of Azactam was injected. A similar degree of damage was seen when a dose of 5 mg L-arginine, an ingredient of Azactam, was injected into the vitreous. CONCLUSIONS: Imipenem and aztreonam are nontoxic to the albino rabbit retina at concentrations that are 500-fold higher than their effective dose against bacterial infection. Azactam is highly toxic at high levels (more than 10 mg injected into the vitreous). Most of the toxicity could be explained by the L-arginine content of the drug.

Animals↗
PubMed1993

The effects of myristyl gamma-picolinium chloride on the rabbit retina: morphologic observations.

PURPOSE: This study was designed to localize the site of action of myristyl gamma-picolinium chloride (MGP) in the rabbit retina and to evaluate the extent of the structural damage induced by the drug. METHODS: The structural damage was assessed at the light microscopic level in eyes treated with various concentrations of MGP at different time intervals after intravitreal injection of the drug. Glial fibrillary acidic protein (GFAP) immunoreactivity was tested in the same eyes and served as an index of retinal damage. RESULTS: The rabbit retinas, examined about 1 mo after MGP injection, exhibited loss of photoreceptors and thinning of the retina in the regions close to the site of injection; remote retinal areas appeared morphologically intact or only slightly affected. Immunocytochemical analysis demonstrated the presence of GFAP in Müller (glial) cells throughout the entire retina. When the effects of MGP were examined at short time intervals (24 and 72 hr) after injection, severe morphologic damage in areas adjacent to the site of drug injection developed in parallel with the electroretinographic findings. However, GFAP could not be demonstrated. CONCLUSIONS: MGP, the preservative used in Depo-Medrol (Upjohn, Kalamazoo, MI), is highly toxic to the rabbit retina.

Animals↗
PubMed1991

The effects of Depo-Medrol preservative on the rabbit visual system.

Periocular injections of corticosteroids play an important role in the management of various ophthalmologic diseases. The Depo-Medrol vehicle, injected into the vitreous, was shown to be toxic to the lens and to the retina when applied at double strength. The authors examined the effects of Depo-Medrol and one of the components of its vehicle, myristyl-gamma-picolinium chloride (MGP), on the functional integrity of the rabbit visual system. Visual function was assessed objectively from the electroretinogram (ERG) and the visual evoked potential (VEP). The experimental drugs were injected into the vitreous humor of one eye while saline was injected into the fellow eye for control. Depo-Medrol did not produce any measurable effects on the ERG or the VEP. When MGP solutions were injected in concentrations at least twice as large as that in the Depo-Medrol, significant reductions in the light- and dark-adapted ERG responses were seen. The effects of the drug on the ERG responses was seen as early as 3 days postinjection and developed to its maximal level within 1-2 weeks. No ERG recovery was seen over a period of more than 2 months. The VEP, elicited by applying light stimuli to the experimental eye, was characterized by low amplitude and delayed implicit time compared with the response obtained from the control eye.

Animals↗
PubMed1989

Uridine diphosphoglucose dehydrogenase activity in normal and osteoarthritic human chondrocytes.

The activity of uridine diphosphoglucose dehydrogenase (UDPGD), a key enzyme in the synthesis of proteoglycans was measured by a quantitative cytochemical method in normal and in osteoarthritic (OA) human cartilage. Normal adult chondrocytes showed low UDPGD activity, which was about half the activity of glucose-6-phosphate dehydrogenase of the same specimens. No significant increase in UDPGD activity was noted in OA chondrocytes. The lack of significantly enhanced UDPGD activity in OA indirectly agrees with studies showing normal 35S uptake in this disease and might explain in part the inability of chondrocytes to cope with continuous proteoglycan loss.

Animals↗
PubMed1988

Photosystem II in Guard Cells of Vicia faba: Immunological Detection.

Antibodies were raised against individual polypeptides of the oxygen-evolving photosystem II (PSII) complex from mesophyll chloroplasts of Vicia faba (Long Pod). These antibodies were used to probe immunologically for the presence of the main structural components of the PSII complex in guard cell chloroplasts, using both immunofluorescence microscopy and Western blotting. Immunofluorescence of epidermal peels with antibodies raised against the extrinsic 33 kilodalton polypeptide, as well as the 47 and the 44 kilodalton subunits and the light-harvesting chlorophyll a/b protein, resulted in intense fluorescence indicating the presence of these polypeptide components in guard cell chloroplasts. Results obtained with Western blot analysis showed that the relative amounts of the 33 kilodalton and light-harvesting complex protein polypeptides are between 60 and 80% of that found in mesophyll cells (on chlorophyll basis). These results provide evidence for the existence of structural components associated with PSII activity in guard cell similar to those of mesophyll chloroplasts.

Journal Article↗
PubMed1985

Immunological evidence for the presence of ribulose bisphosphate carboxylase in guard cell chloroplasts.

Ribulose bisphosphate carboxylase (Rubisco) has been found in Vicia faba L. guard cell chloroplasts by two immunological methods, using antibodies raised against highly purified subunits of ribulose bisphosphate carboxylase. Indirect cytoimmunofluorescence revealed binding of antibodies against both the small and the large subunits of ribulose bisphosphate carboxylase. Binding was observed only after partial digestion of guard cell walls by 4% Cellulysin to facilitate antibody penetration. After electrophoresis of a homogenate of guard cell protoplasts, the presence of both subunits was also revealed by immunolabeling technique. Positive response required the inhibition of proteolysis which appeared to be active upon homogenization.

Journal Article↗
PubMedDate not supplied

NADPH diaphorase activity in mammalian retinas is modulated by the state of visual adaptation.

NADPH diaphorase histochemistry is commonly used to identify cells containing nitric oxide synthase (NOS), the enzyme catalyzing the production of nitric oxide from L-arginine. NADPH diaphorase activity and NOS immunostaining was demonstrated in different cells of the vertebrate retina; photoreceptors, horizontal cells, amacrine cells, ganglion cells, and Müller cells. However, the physiological role of nitric oxide (NO) in the retina has yet to be elucidated. In this study, we tested the assumption that NADPH diaphorase activity in the retinas of rabbits and rats depended on the state of visual adaptation. In the rabbit, light adaptation enhanced NADPH diaphorase activity in amacrine cells and practically eliminated it in horizontal cells. Dark adaptation induced the opposite effects; the NADPH diaphorase activity was reduced in amacrine cells and enhanced in horizontal cells. Retinas from eyes that were injected intravitreally with L-glutamate exhibited a pattern of NADPH diaphorase activity that was similar to that seen in dark-adapted retinas. In rats, the NADPH diaphorase activity of amacrine and horizontal cells exhibited adaptation dependency similar to that of the rabbit retina. But, the most pronounced effect of dark adaptation in the rat's retina was an enhancement of NADPH diaphorase activity in Müller cells, especially of the endfoot region. Assuming that NADPH diaphorase activity is a marker for NOS, these findings suggest that NO production in the mammalian retina is modulated by the level of ambient illumination and support the notion that NO plays a physiological role in the retina.

Adaptation, Ocular↗