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)

A morphological classification indicating the stage of the prevention of aldose reductase inhibitor (ARI) on the rat galactosemic cataract was investigated. Three week old rats (body weight 50 g) were fed with a 25% galactose diet. Two kinds of ARIs (ADN-138, FR-74366) were used with a different dose 25% galactose fed each drug. The rats on the 25% galactose diet rapidly developed cataracts in the equatorial region of the lens followed by total cataracts. The morphological processes of the galactose cataracts receiving preventive treatment of ARI were divided into 5 types according to their intensity.
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PMID:[Morphological classification of the prevention by aldose reductase inhibitor of rat galactosemic cataract]. 250 49

In experimental galactose cataract of rats, lens fiber cells were gradually destroyed by swelling and liquefaction occurring due to the accumulation of galactitol. In addition to the destruction of lens fiber cells, marked regeneration of lens epithelial cells was universally observed. In this study, we used the technique of 3H-thymidine autoradiography and examined the movement of regenerated (DNA synthesis) lens epithelial cells. On the fourth day from the starting of 50% galactose chow, 3H-thymidine was injected into the anterior chamber. After one week, 3H-thymidine-labelled epithelial cells was observed at the bow region of the equatorial area. After 2 to 4 weeks, labelled cells were found in the regenerated lens fibers of the cortex. After 3 weeks, labelled cells about to be destroyed by swelling and liquefaction were recognized. However, a few labelled cells were still observed in the epithelial cell layer. The same experiments were performed in two groups of normal chow-fed one and 50% galactose + an aldose reductase inhibitor (Statil)-fed one. The movements of 3H-thymidine labelled epithelial cells in the above two groups were almost identical. In addition, the movement of labelled cells was normalized by an aldose reductase inhibitor.
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PMID:[Movement of regenerated lens epithelial cells in 50% galactose cataract and an aldose reductase inhibitor]. 251 12

Five hundred patients undergoing cataract surgery were prospectively examined, and 46 Caucasian patients were found to have strictly idiopathic cataracts severe enough to warrant surgery on or before age 55. In a masked fashion we determined the activity of galactokinase (GK) and galactose-1-phosphate uridyl transferase (GPUT) in these patients as well as on 53 age matched controls. With respect to GK no cataract patient had an enzyme level of less than 2 standard deviations below the control mean. However, 3 of 45 (6.7%) patients in the cataract group had a GPUT level less than 2 standard deviations below the mean for controls, and were presumably heterozygotes for this enzyme. In comparison with the expected population rate of 0.8% this is highly significant (p = 0.006). Abnormalities in galactose pathway enzymes may therefore predispose to development of presenile cataracts. In affected people there is a possibility of treating these patients clinically by dietary restriction of dairy products or by using aldose reductase inhibitors to prevent or reverse cataract formation.
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PMID:Idiopathic presenile cataract formation and galactosaemia. 253 52

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

The lens myo-inositol (MI) content is known to be depleted during initial cataractogenesis in both streptozocin (STZ)-induced diabetic and 50% galactose-maintained rats. The objective of this study is to establish whether dietary MI supplementation protects lens transparency, MI content and individual fiber cell ultrastructure is both model systems of sugar cataract. In the diabetic study, after induction with STZ, rats were immediately placed on normal chow supplemented with 2% MI for 14 weeks while additional age-matched control and diabetic rats remained untreated. Within 14 weeks, untreated diabetic rat lenses were totally opaque with undetectable MI content; MI was undetectable by 1 month. These opaque lenses were devoid of fiber cells and exhibited only acellular, amorphous cortical regions between 0 and 500 microns from the capsule. In contrast, 14-week, MI-treated diabetic rat lenses exhibited only cortical vacuolation indicative of initial cataractogenesis; MI content was 0.41 +/- 0.26 mumol/g wet weight of lens. Scanning electron micrographs indicated a granulated, acellular region subadjacent to the capsule and confirmed the presence of cortical fiber cells, approximately 100 microns from the capsule. In 50% galactose-maintained rats, daily administration of MI for 1 month was unable to prevent total opacification or reverse initial cataractogenesis indicating that in rapidly progressing galactose cataracts, MI was unable to protect lens transparency, MI content and cortical fiber ultrastructure. The combined results suggest that MI may exert a protective effect on the slowly developing diabetic cataract. Of the 2 models, the time course and polyol content in STZ diabetic lenses more closely correlate to the human diabetic lens which has a low activity of aldose reductase; therefore, it is possible that MI may exert a protective effect in human diabetic cataract.
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PMID:Dietary myo-inositol effect on sugar cataractogenesis. 258 18

Classical galactosemia due to a deficiency of galactose-1-phosphate-uridyl transferase, is an autosomal recessive disorder of galactose metabolism with an incidence in Ireland of one in 30,000 births. It can result in cataract formation through the accumulation of galactitol within the lens. Seventeen children with transferase deficient galactosemia were studied. Early diagnosis followed by a galactose-free diet and tight biochemical control prevented cataract formation in 13 cases after a mean follow-up of 6.3 years. Cataracts did not regress in all patients commenced on diet by 6 weeks but early treatment prevented progression. The ophthalmologist may play an important role in the monitoring of patients with this disease as the recognition of new lens opacities by slit-lamp biomicroscopy may be the most sensitive initial index of inadequate biochemical control.
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PMID:Ophthalmic findings in classical galactosemia--a screened population. 276 Jul 88

Raman spectroscopy shows that maturation of galactose cataract greatly increases the water signal (at 3417 cm-1) which is correlated with the inbibition of water in the lens. The maximum water: protein ratio (expressed as Raman intensity ratio I3417:I2936) occurs at the peripheral cortex (i.e. approximately 4.7), which is much higher than the ratios found in Emory cataract (approximately 0.3) and in cac-strain mouse cataract (approximately 0.5). It is demonstrated that Raman measurement of the intensity ratio I3417:I2936 is a more sensitive way to reflect increase of water in cataract, compared to water concentration (percentage of wet weight of the lens). The small decrease in the sulfhydryl profile along an equatorial diameter is attributed to the concentration decrease in glutathione. There is no spectroscopic evidence for extensive disulfide bond formation associated with galactosemic cataractogenesis in rat. There is an increase in the tyrosine I832:I858 ratio (normal 1.74; cataract 3.43), indicating a strengthening of the phenolic hydrogen bond, a change which has been found in Raman spectra of all cataracts studied. A comparison of the Raman spectra of normal lenses and mature cataracts reveals no change in conformation of the protein backbone.
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PMID:Galactose-induced cataract in rat: Raman detection of sulfhydryl decrease and water increase along an equatorial diameter. 280 22

Using a 31P-NMR spectroscopy, we monitored the metabolic kinetics of energy organophosphate compound in rat lens during the process of generating galactose cataract. The most remarkable metabolic change in the earlier phase of galactose cataract formation was found in alpha-glycerophosphate. This increased significantly, as compared to controls, since the day 3 of giving feed containing 25% galactose. The high level lasted for up to three weeks, decrease followed by a gradual decrease and subsequently a significant decrease at five weeks. Adenosine triphosphate (ATP) showed a significant decrease in the galactose group compared to the controls from two weeks after beginning of the experiment and the decrease continued. Inorganic orthophosphate increased gradually in the galactose group as compared to the controls, the increase being of significance at one week reading a maximum at two weeks followed by a subsegment decrease. Our basic study suggests that 31P-NMR spectroscopy is a useful technique in lens of the metabolic kinetics, to noninvasively determine the pathophysiology of galactose cataract, which has been studied biochemically and histologically.
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PMID:[A study on the metabolism of galactose cataract using a 31P-NMR spectroscopy]. 281 81

In order to obtain an experimental model for studying inherited disorders of galactose metabolism in man, we administered to adult rats a diet supplemented with 50% of galactose during 38 days. The results showed clinical symptoms such as polyuria, polydipsia, growth retardation and bilateral cataract. The main biochemical features were an increase in the galactokinase and uridyltransferase activities in liver, an ubiquitous accumulation in tissues and a considerable urinary elimination of galactose and galactitol, a weak accumulation of galactose-1-phosphate in tissue and a hyperaminoaciduria. This work led us to quantify the respective importance of the major pathway and minor pathways of galactose in the rat after a galactose-rich diet.
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PMID:Metabolic studies of a sustained galactose overload in rat. 282 61

Galactose, and the phosphorothioates, WR-77913 and WR-2721, which inhibit cataract produced by X-irradiation, were evaluated for their effects on the phase separation temperature, Tc, of calf lens homogenate. The reagents were added to nuclear homogenate and the change in Tc per mol, dTc/dC, was measured. Galactose decreased Tc, -65 degrees C mol-1, WR-77913 decreased Tc, -28 degrees C mol-1 and WR-2721 decreased Tc, -76 degrees C mol-1. These are the first phase separation inhibitors that can be used in vivo to study the inhibition of lens opacification.
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PMID:Inhibition of phase separation by reagents that prevent X-irradiation cataract in vivo. 282 97


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