Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the pathological changes of the ciliary body in Royal College of Surgeons (RCS) rats with an inherited retinal degeneration. Morphometric analyses were performed on sectioned ciliary bodies by a computerized morphometry system. Age-matched non-pigmented Sprague-Dawley (SD) rats were used as the control animals. The ciliary body of 26-day-old RCS dystrophic rats showed normal structure. However, the length and height of the pars plicata of the ciliary body became shorter and the area became smaller with increased age. Significant decreases in the values of these three parameters were observed between 26-day-old and 3-month-old RCS dystrophic rats. These parameters also showed significant differences when values of 3-month-old RCS dystrophic rats were compared to those of 3-month-old control SD rats. The same trends were observed in the ciliary body measurements in RCS dystrophic rats up to 1 year of age. Scanning electron microscopic examination demonstrated the progressive thinning of the pars plicata of the ciliary body with age in the RCS dystrophic rats. The total volume of the ciliary process of 6-month-old RCS dystrophic rats appeared to be one-half that of 26-day-old RCS dystrophic rats. Transmission electron microscopy revealed progressive cellular degenerative changes in the non-pigmented and pigmented ciliary epithelium of the RCS dystrophic rats. It was apparent that the pigmented ciliary epithelium had more severe degenerative changes than the non-pigmented ciliary epithelium. Immunostaining for Na+ + K+ ATPase of the ciliary epithelium was found to be less in the RCS dystrophic rats than in age-matched controls. This result suggests a possible dysfunction of ion transport in the ciliary body of the RCS dystrophic rats, which may account for their increased incidence of cataract formation. Although the mechanisms for the ciliary body degeneration in RCS dystrophic rats remain speculative, these findings add a new area of interest in this model of inherited retinal dystrophy.
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PMID:Ciliary body degeneration in the Royal College of Surgeons dystrophic rat. 164 4

Selenite (Se) cataract in rabbit lenses was investigated in vitro to define target sites of Se that might be involved in calcium elevation and lens opacification. Experiments in which the anterior or the posterior surface of the lens was exposed to Se showed that anterior exposure led to ionic imbalances and opacification in the whole lens. Posterior exposure to Se (1 mM, 2 hr) had no effect. Se treatment (0.1 mM) of epithelial homogenates led to a 56% loss of thiol (SH) groups, and treatment of lenses cultured in Se led to a 22% loss. Experiments to assess the effects of Se on SH groups of Ca-ATPase showed that the transport enzyme was not affected by the poison. To determine whether this negative finding was due to the lack of accessibility of Se for SH sites in an ordered membrane, Ca-ATPase was also assayed in homogenate preparations treated with Se; still no inhibition of Ca-ATPase activity was observed. Therefore, an alternative explanation of calcium elevation was explored. The passive movement of labeled chloride (36Cl) was found to be twice as fast in Se-treated lenses as it was in control lenses. Measurement of the lens voltage indicated an 18-mV depolarization in Se-treated lenses, suggesting that Se increased membrane permeability. All cataractogenic changes that occurred after Se treatment were irreversible-despite intervention with external application of reduced glutathione or cysteine. This finding suggests that irreversible loss of SH groups in lens membranes is important in maintaining ion homeostasis.
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PMID:Effect of selenite on epithelium of cultured rabbit lens. 182 4

Three newly detected dominant cataract mutations (Asc-1, Cat-3vao, Tcm) were investigated for effects on osmotic alterations in the lenses of heterozygotes. The lens wet weight was reduced in two mutant lines (Cat-3vao and Tcm), and the water content in the lenses of the Cat-3vao mice was increased. Moreover, in the cataractous lenses from Cat-3vao mice, the sodium-potassium-adenosine triphosphatase (Na(+)-K(+)-ATPase) activity was enhanced and the ATP concentration, correspondingly decreased. The osmotic variations observed in the Cat-3vao mutants might have been due to a metabolic response to the yet unknown, primary pathological event. The lenses of the other two mutant lines (Asc-1 and Tcm) revealed no alterations that could be related to osmotic stress. In no mutant line investigated could a decrease in Na(+)-K(+)-ATPase activity be demonstrated that was similar to the causative factor in the Nakano mutant line. The Cat-3vao mice exhibited some similarities to the Philly mutant line.
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PMID:Osmotic state of lenses in three dominant murine cataract mutants. 216 48

The Nakano mouse is a hereditary cataract model whose most characteristic change is a deficiency in lens Na+,K(+)-ATPase. Consequently, there is a change in lenticular sodium and potassium ion levels just before cataract formation. The amounts of calcium ion also change suddenly in the lens, with accumulated levels higher than any other type of cataract. Other biochemical changes coincide with the development of lens opacity, including decreases in the levels of reduced glutathione, ATP, biosynthetic activity of proteoglycans in epithelial cells, and the permeability of gap junction channels in fiber cells. The decrease in the activity of Na+,K(+)-ATPase results in changes in a number of key metabolic parameters, resulting in the eventual opacification of the Nakano mouse lens at approximately 30 days of age.
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PMID:Hereditary cataract of the Nakano mouse. 219 7

Our earlier studies of cataracts in Dahl salt-sensitive (DS) rats suggested the possibility of altered lens ion transport as a contributing factor in cataractogenesis in this genetic model. We also observed that those weanling DS rats with the greatest pressor response to a high salt diet eventually developed cataracts, and that changes in salt intake modified cataract formation. In the present studies, we measured lens 86Rb uptake as an index of sodium-potassium adenosine triphosphatase [(Na+,K+)-ATPase] activity in weanling DS rats before the development of cataracts or sustained hypertension. Additionally, plasma renin activity was measured to indirectly assess our hypothesis that the difference between cataract-prone DS rats and DS rats unlikely to develop cataracts might be a difference in degree of salt sensitivity. At the age of 4 weeks, 50 DS and 25 salt-resistant (DR) rats were given a high sodium diet for 2 weeks, at which time the rats were divided into three groups based on the systolic blood pressure response, that is, cataract-prone DS rats with systolic blood pressure equal to or greater than 155 mm Hg, DS rats unlikely to develop cataracts with systolic blood pressure less than or equal to 125 mm Hg, and DR rats. Lens and aqueous humor Na+ and K+, lens dry weight, and water content were not significantly different among the three groups of weanling rats. Plasma renin activity was lowest in cataract-prone DS rats and low in DS rats unlikely to develop cataracts when compared with values in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lenticular rubidium uptake and plasma renin activity in weanling cataract-prone salt-sensitive rats. 240 57

A material with inhibitory action to Na+/K+ ATPase was found in the lens of the ICR/f rat, a recessive hereditary cataractous rat. The material also induced lens opacification in vitro. From the results of amino acid analysis and by secondary ion mass spectroscopy, it was suggested that the material might contain approximately equimolar amounts of four amino acids, ie, aspartic acid, serine, glutamic acid and glycine, and that the molecular weight was 444. These facts suggested that this material with Na+/K+ ATPase inhibitory action might be a peptide. However, there is not yet any corroborating evidence to show whether this peptide is only a single material or not. The peptide significantly increased with aging in the lens of the ICR/f rat until approximately 90 days, when cataract became manifest, but its content decreased thereafter. This study suggests that one of the causes of cataractogenesis in the ICR/f rat might be this peptide, which is transformed in the lens with aging, and also that the peptide might accelerate lens opacification after cataractogenesis.
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PMID:Characterization of peptide inducing cataractogenesis in lens of hereditary cataractous rat (ICR/f RAT). 255 1

Our recent investigations have shown that the Eisai compound, E-0722, (2R-4S-6-fluoro-1-2-methylspirochroman 4,4'-imidazolidine 2,5'-dione) is a more potent aldose reductase inhibitor than Sorbinil (D-6-fluorospirochroman 4,4'-imidazolidine 2,5'-dione). In the previous studies these aldose reductase inhibitors were added to the 50% galactose diet fed to rats to determine their effect on galactose-induced alterations in the lens and the development of cataract. In this report we present our results on the effect of prefeeding the aldose reductase inhibitor, E-0722, on the alterations in rat lens following subsequent feeding of galactose. For this study, young Sprague Dawley rats were prefed either rat chow or rat chow plus 50% galactose containing 1mg/day/Kg body weight of E-0722 for 1 or 2 weeks. After this dietary regimen, the animals were transferred to diets containing 50% galactose for different periods. For controls, rats were fed either rat chow or 50% galactose without the prefeeding of E-0722. Our results obtained through gross observation of the lenses, light microscopic studies of lens sections and assay of Na+-K+-ATPase (NPPase) activity show that the prefeeding of E-0722 prior to galactose feeding delays galactose-induced alterations and the development of mature cataract.
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PMID:Prefeeding of aldose reductase inhibitor and galactose cataractogenesis. 255 45

Cataractogenesis was studied in young rats homozygous for the radiation-induced recessive cataract mutation cat. Homozygous cat/cat rats have reduced body weight (about two-thirds of the wild type) when 3 weeks old. The litter size is also diminished to about two-thirds of the wild type. For lens-specific parameters, as compared with homozygous wild type, the wet weight of the cataractous lenses is reduced, although the concentration of water-soluble lens proteins per wet weight is the same. No major alterations could be detected in the pattern of the water-soluble lens proteins separated by isoelectric focusing or gel electrophoresis run with or without mercaptoethanol. Additionally, no statistically significant alterations could be detected in the biochemical parameters of the lens used as indicators for osmotic stress (water content of the lens and the Na+-K+-dependent ATPase), for the energy state (ATP) and for the redox state (oxidized glutathione and superoxide dismutase). In contrast, the activity of transglutaminase is significantly enhanced in lenses as well as in the liver of young cat-rats, which might be understood as a biochemical marker for alterations in the developmental program. Cataractogenesis in the cat-rat is, therefore, suggested to be part of a syndrome including dwarfism and reduced litter size.
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PMID:Biochemical analysis of young rats homozygous for the cataract mutation cat. 256 75

The autosomal, dominant mutation Scat (suture-cataract) was found in (101/El x C3H/El)F1-hybrid mice. The severity of the cataract is dependent on the gene dose. The mutation causes an anterior suture opacity in heterozygotes amd microphthalmia with vacuolated lenses in homozygotes. In histological sections of lenses the heterozygotes exhibit a hydropic swelling of lens epithelium, whereas in homozygotes interruption and degeneration of lens fibers as well as clefts and folds of the capsule were observed. The mutation has a complete penetrance and constant expressivity. The body weight of the mutants is not altered; the mutation has no effects on fertility or viability. The lens wet and dry weights are diminished (more pronounced in the homozygotes). The water content of the lens is enhanced only in the homozygous Scat mutants. Biochemically, the lenticular content of water-soluble proteins is decreased in the homozygous Scat mutants. By electrophoresis, in the lenses of homozygous Scat mutants a different pattern of water-soluble proteins could be observed. The lenses of both, heterozygous and homozygous Scat mutants exhibit enhanced Na+,K+-ATPase activity and a decreased ATP concentration. The genetical, morphological or biochemical data suggest that the effect of the Scat mutation is distinct from other described cataract mutations in mice.
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PMID:Characterization of Scat (suture cataract), a dominant cataract mutation in mice. 279 38

We have previously reported a high incidence of cataract formation in adult hypertensive salt-sensitive rats, suggesting that hypertension may be an important cataractogenic risk factor. Weanling salt-sensitive rats that eventually developed cataracts showed a marked increase in the pressor response to a high-sodium diet compared to salt-sensitive rats that did not develop cataracts. A lens and aqueous fluid electrolyte imbalance occurred in all adult salt-sensitive rats examined, but was greater in the salt-sensitive rats that developed cataracts, suggesting an alteration in lens and/or ciliary ion transport in cataracts associated with hypertension. In the present study, lens 86Rb uptake was measured in adult hypertensive salt-sensitive rats prior to cataract formation. 'Cataract-prone' salt-sensitive hypertensive rats (increased pressor response to a high sodium diet given at weanling age), salt-sensitive hypertensive rats unlikely to develop cataracts and control salt-resistant rats were studied at the age of 16 weeks. Total and ouabain-insensitive lens 86Rb uptake were measured for the determination of ouabain-sensitive uptake, an index of Na+,K+-ATPase activity. Lens ouabain-sensitive 86Rb uptake was low in adult hypertensive cataract-prone salt-sensitive rats before cataract formation compared with values in control resistant rats. Intermediate values were observed in hypertensive salt-sensitive rats unlikely to develop cataracts. These data suggest that altered ion transport may play a pivotal role in cataractogenesis associated with this model of hypertension. The data are also consistent with the concept of a generalized defect in epithelial ion transport, at least in salt-sensitive hypertension.
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PMID:Lenticular rubidium uptake in hypertensive 'cataract-prone' salt-sensitive rats. 285 35


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