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)

In this study, we used ICR (Institute of Cancer Research) strain mouse because they showed hypergalactosemia but not cataractogenesis. We examined the proliferative ability of the lens epithelial cells by means of a whole-mount preparation of epithelium and 3H-thymidine autoradiography. An increased number of labelled cells was not found in the mouse. The increased proliferative ability of epithelial cells in rat galactose cataract did not seem to be caused by hypergalactosemia.
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PMID:[Cell kinetics of lens epithelial cells on the whole-mount preparation (3). Changes in mouse cataract lens by feeding galactose]. 155 78

The effect of pyruvate on the progress of galactose cataract has been studied. Pyruvate was administered topically in the form of eye drops. Such treatment was found to delay the onset of the cataractous changes. Cataract formation was studied by visual inspection with pen light, as well as with slit lamp biomicroscopy in the intact animal. The delay in the formation of cataract was associated with the preservation of the levels of lens ATP, soluble proteins and the decreased accumulation of galactitol. In vitro organ culture experiments yielded similar results.
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PMID:Prevention of galactose cataract by pyruvate. 159 5

Attenuation of both the active transport of myo-inositol and Na(+)-K(+)-ATPase pumping activity has been implicated in the onset of sugar cataract and other diabetic complications in cell culture and animal models of the disease. Cultured bovine lens epithelial cells (BLECs) maintained in galactose-free Eagle's minimal essential medium (MEM) or 40 mM galactose with and without sorbinil for up to 5 days were examined to determine the temporal effects of hypergalactosemia on Na(+)-K(+)-ATPase and myo-inositol uptake. The Na(+)-K(+)-ATPase pumping activity after 5 days of continuous exposure to galactose did not change, as demonstrated by 86Rb uptake. The uptake of myo-[3H]inositol was lowered after 20 h of incubation in galactose and remained significantly below that of the control throughout the 5-day exposure period. The coadministration of sorbinil to the galactose medium normalized the myo-[3H]inositol uptake. No significant difference in the rates of passive efflux of myo-[3H]inositol or 86Rb from preloaded galactose-treated and control cultures was observed. Culture-media reversal studies were also carried out to determine whether the galactose-induced dysfunction in myo-inositol uptake could be corrected. BLECs were incubated in galactose for 5 days, then changed to galactose-free physiological medium with and without sorbinil for a 1-day recovery period. myo-Inositol uptake was reduced to 34% of control after 6 days of continuous exposure to galactose. Within 24 h of media reversal, myo-inositol uptake returned to or exceeded control values in BLECs switched to either MEM or MEM with sorbinil.2+ reversible and occurred independently of changes in Na(+)-K(+)-ATPase pumping activity in cultured lens epithelium, indicating that the two parameters are not strictly associated and that the deficit in myo-inositol uptake occurs rapidly during hypergalactosemia.
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PMID:Uncoupling of attenuated myo-[3H]inositol uptake and dysfunction in Na(+)-K(+)-ATPase pumping activity in hypergalactosemic cultured bovine lens epithelial cells. 164 82

Our previously reported investigations showed that cataracts could be induced in fetal lenses through the maternal feeding of galactose during pregnancy. We also reported that the lens opacity present at birth reverses completely by 30 days of age if there is no further post-natal exposure to galactose. This investigation was designed to investigate if an aldose reductase inhibitor (ARI) has any cross-placental effect in preventing galactose-induced cataracts in fetuses. We have also evaluated if there are any milk-mediated effects of galactose on cataract induction and of galactose and ARI on the maintenance or reversal of opacities induced in utero. Pregnant Sprague-Dawley rats were fed either 50% galactose or rat chow with or without the ARI, (2R,4S)-6-fluoro-2-methyl spirochroman-4,4'-imidazolidine-2',5'-dione (Eisai compound E-0722). Following parturition, pups of mothers from the different dietary groups were either fed by their own mothers or foster fed by lactating females fed either rat chow or 50% galactose with or without the ARI. Lenses of the pups were examined at desired intervals with light and scanning electron microscopes. We observed that: (a) both galactose and the ARI had a cross-placental effect on the fetal lenses in the development and inhibition of cataracts, respectively; (b) galactose had very little, if any, milk-mediated effect on either the induction of cataracts in newborn pups that were born with transparent lenses or the maintenance of cataracts induced in utero; (c) the ARI appeared to have a milk-mediated effect, which accelerates the reversal of cataract associated alterations in lenses of pups with cataracts induced in utero, leading to further reinstatement of lens transparency; and (d) the presence of ARI in the diet of rats during pregnancy and/or post-parturition provided continued protection to the lenses of pups that were exposed to a galactose diet following birth.
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PMID:In utero and milk-mediated effect of aldose reductase inhibitor on galactose cataracts. 174 65

Aldose reductase inhibitors (ARIs) have been known to be effective in preventing galactose cataract by blocking the polyol pathway. Because the rat congenital galactose cataract is also induced by accumulated polyol, the effect of an ARI in the induction of congenital galactose cataract was investigated. Pregnant rats were placed on a 30% galactose diet. On fetal day 16, 17, 18 or 20, the fetal lenses were examined by light microscope. Lenses from newborn rats with mothers fed galactose diet until gestational day 16, 17, 18 or 20 and then given a galactose diet containing ARI were also examined. The fetal lenses obtained from galactose-fed mother rats on day 16 of gestation were morphologically similar to those of controls. On day 17, the experimental lenses displayed vacuolated areas. The lenses of newborn rats with mothers given an ARI diet after gestational day 16 showed no morphological changes, while a few small vacuoles were observed in the lens of rats with mothers given the ARI diet after day 17, 18 or 20 of gestation. ARI inhibited the rat congenital galactose cataract even when the drug was given to the mother rat during a late stage of pregnancy.
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PMID:Inhibition in rat of development of in utero galactose-induced cataract by an aldose reductase inhibitor--a light microscopic study. 177 Jun 72

In connection with the increased incidence of cataract in middle-aged patients investigations were carried out in order to clear up one of the possible causes of this condition. The detection of a substantial decrease of galactose-1-phosphate uridyl transferase activity in patients with presenile cataract evidences the disturbance of galactose metabolism these patients and allows to accept this genetic defect as the causes of opacification of the lens. Attention was called to the eventual importance of these investigations because of the adoption of a diet without galactose in person threatened+ by cataract could prevent or check this disease.
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PMID:[Study of galactose-1-phosphate uridyltransferase activity in erythrocytes of patients with presenile cataract]. 181 55

The activity of red blood cells galactose-1-p-uridyl transferase (GPUT) was determined by the spectrophotofluorometric method. The average GPUT activity in 102 control subjects was 13. 34 +/- 2. 03u. There were no differences in the sexes and ages. The average GPUT activity in 108 patients with congenital cataract was 11.58 +/- 4. 03u and was lower than that of the controls (P < 0.01). The GPUT activity in 14 of the 108(12.96%)patients was all-3SD below the mean value of the controls (< 7.24u) and the range was from 4.02u to 7.13u with the mean value of 5. 93u being about 44.45% of the normal. The difference between the two groups was statistically significant (P < 0.001). The results indicated that some of the patients with congenital cataract were due to decrease in the GPUT activity. The patients with decrease GPUT activity were mainly suffering from cataracts and their systemic disease were mild.
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PMID:[Galactose-1-phosphate uridyl transferase and congenital cataract]. 184 60

A comparative study of the metabolic kinetics of organophosphate compounds, biochemical changes and histological changes, in the rat lens during the process of the generating galactose cataract. The change of alpha-glycerophosphate (alpha-GP) with time was analogous to that of dulcitol and the decrease of alpha-GP depended on histological destruction. Furthermore phosphorylcholine decreased considerably before adenosine triphosphate (ATP) decreased, the latter commencing when the histological destruction of the lens progressed to all around the lens. In addition, inositol decreased rapidly after ingestion of galactose. It was concluded that the decrease of alpha-GP was caused by the flow from the lens, and the decrease of ATP started from the epithelium in the lens. Therefore, it was speculated that the decrease of inositol was caused by decrease in the active transport of inositol.
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PMID:[Relation between metabolic and histological changes in the rat lens during the pathogenesis of galactose cataract]. 187 20

In order to investigate the effect of age on the rat galactosemic cataract, 3, 6, 12 and 24-week-old rats were fed with a 50% galactose diet. The cataractous lenses were observed by light microscopy, and the amount of galactitol measured. All rats fed with 50% galactose developed cataracts in the equatorial region. However, the morphological and biochemical development of the galactose cataract in old rats was slower than in young rats. These results suggested that older diabetic patients are less likely to develop diabetic cataract than younger patients.
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PMID:[The influence of aging on the development of rat galactosemic cataract]. 189 53

In this review, the relationship between lactose and human cataract is examined from the presently available biochemical, metabolic, and epidemiological data. The exceptional cases of homozygous enzyme deficiency being excluded, fragmentary data give reason to believe that a risk of cataract secondary to lactose and galactose ingestion is present in certain subpopulations. In these population groups, the size of which is unknown, the lens could be exposed to intermittent episodes of hypergalactosemia due to the presence of a partial enzyme deficiency in the galactose metabolic pathway, and/or the persistence of a high adult jejunal lactase activity, and/or to a large and repeated consumption of either whole lactose or easily absorbed lactose (hydrolyzed forms and nonpasteurized yogurt).
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PMID:Lactose and cataract in humans: a review. 190 25


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