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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Age-related cataract is a condition characterized by multiple mechanisms and multiple risk factors. The mechanisms that bring about a loss in transparency include oxidation, osmotic stress, and chemical adduct formation. Risk factors for cataract include diabetes, radiation (ultraviolet B, x-ray), certain pharmaceutical substances, certain nutritional states, and possibly acute episodes of dehydration. Interaction occurs between and among mechanistic factors and risk factors. Thus nutrition must be considered as one part of a tapestry of intertwined events and responses. Certain experimental models for nutritional cataract have been useful for study of the cataractogenic process but are probably not important factors in the human disease. Little current evidence supports significant roles in human senile cataract for imbalances of tryptophan or other amino acids, deficiencies of calcium or selenium, or excessive intake of selenium. Overconsumption of galactose is likely to be hazardous only in subjects with genetic inability to metabolize this sugar. Vitamins with antioxidant potential (riboflavin, vitamin E, vitamin C, carotenoids) deserve further research scrutiny to ascertain their significance in cataract etiology. Excessive caloric intake needs to receive added emphasis as a factor contributing to cataract. Diabetes increases the likelihood of cataract three- to four-fold. Obesity, defined as more than 20% overweight, is considered a major risk factor for non-insulin-dependent, or type II, diabetes (69, 73). Weight control can be recommended as a prudent, safe, economic, and effective means of lowering risk probability for diabetes and the associated complication of cataract.
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PMID:Nutritional factors in cataract. 220 Apr 64

Experimental diabetic and galactosemic animal models are widely used to study diabetes-induced complications. Galactose feeding can rapidly produce cataract, retinopathy and nephropathy; it is therefore favored over the diabetic model. Although the common feature for both models is the activation of aldose reductase, there are substantial differences between the two--not only does the rate of cataract progression differ but the metabolic patterns are far more complex than for polyol production alone. We here present the result of a comparison between diabetic and galactosemic lenses and show the differences in phosphorus and aldose metabolism, cell integrity and osmotic environment.
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PMID:Metabolic studies of galactosemic cataract. 220 47

Cataracts were produced in rat lenses by either feeding a diet containing 50% galactose or by inducing diabetic condition by intravenous injection of streptozotocin. Proteolysis of crystallins, protease activity of calpain II enzyme (EC 3.4.22.17), and presence of calpain molecule (antigen) were determined at four cataract stages--I, cortical vacuoles, II, vacuoles plus hazy cortex, III, nuclear cataract, and IV, mature cataracts. Calpain activity was normal or moderately elevated at early stages of galactose and diabetic cataracts. Later stages III and IV showed proteolysis of lens crystallins, increased proportion of insoluble proteins, loss of calpain enzyme activity and calpain molecule from the soluble fraction, and reduced amounts of calpain associated with insoluble pellet. In galactose cataract, the largest increase in lens calcium were found when proteolysis was present. These results provide evidence for calpain-induced proteolysis of lens crystallins in two in vivo models of sugar cataracts in rodents.
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PMID:Calpain II in two in vivo models of sugar cataract. 220 51

Gangliosides were isolated from human senile cataractous lenses by solvent extraction, DEAE-Sephadex column chromatography, and thin-layer chromatography. The content and composition of gangliosides were examined in individual lens tissues. Three predominant gangliosides, GM3, GM1, and GD1a, were tentatively identified in comparison with authentic brain gangliosides, and several unidentified gangliosides were also recognized. The increase in ganglioside content per mg of protein content in cataractous lenses was found to be influenced by two physiologic parameters: aging and cataract progression. The mature cataractous lenses showed a higher ganglioside level on a protein basis than the immature lenses compared with the same age group. On the basis of statistical analysis, an age-dependent increase in ganglioside concentration was recognized in both mature and immature lens groups. The relative increase in slow-moving polysialogangliosides on thin-layer chromatography seemed to be caused by the maturation of cataract. The sugar composition of one of the polysialogangliosides was found to be glucose, galactose, and sialic acid in the molar ratio of 2:1:4; this suggests the presence of a unique ganglioside species in human cataractous lens.
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PMID:Increase in lens gangliosides due to aging and cataract progression in human senile cataract. 221 Oct 13

Cataract, the major cause of blindness world-wide, may be caused partly by modification of lens proteins by carbamylation and non-enzymic glycosylation (glycation) in some patients. Aspirin has been found to protect against these modifications and to prevent cyanate-induced opacification occurring in whole rate lenses. Ibuprofen is an aspirin-like anti-inflammatory drug which appeared as a protective factor against cataract in an Oxford case-control study. The binding of cyanate, galactose and glucose 6-phosphate to lens proteins, and the effect of ibuprofen on this reaction was investigated, as was cyanate-induced opacification in whole rat lenses. Labelled metabolite was incubated with bovine lens homogenate in the presence and absence of ibuprofen, and the incorporation of label into the lens homogenate was followed. Simultaneous and preincubation experiments were performed. Intact rat lenses were incubated in culture medium with and without cyanate and ibuprofen. The phase separation temperature was noted as the temperature at which opacity first appeared on cooling. Cyanate, galactose and glucose 6-phosphate bind progressively to lens proteins. Simultaneous incubation with ibuprofen reduces cyanate and galactose binding but not glucose 6-phosphate. Ibuprofen protects against opacities due to cyanate-induced phase separation. Ibuprofen has protected against cataract in the models of cataractogenesis in this study. It appears to have a different mechanism of action from that of aspirin. These studies provide some support for the idea, based on epidemiological findings, that ibuprofen might be a useful anti-cataract drug.
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PMID:Ibuprofen, a putative anti-cataract drug, protects the lens against cyanate and galactose. 231 79

Rats fed a high galactose (30% galactose) diet (w/w) or made diabetic by injecting streptozotocin developed mature cataracts in approximately 45 and 90 days, respectively. Addition of allopurinol, a commonly used drug in the therapy of gout, to the high galactose diet or to the normal diet fed to diabetic rats advanced cataractogenesis in both the groups by approximately 50%. Allopurinol fed to control rats did not cause cataract formation. Feeding butylated hydroxy toluene (BHT), an antioxidant, prevented the allopurinol-induced advancement of cataract formation in galactosemic and diabetic rats. Assuming that these results are applicable in human subjects, there is need for caution in using allopurinol for the therapy of gout in diabetic subjects.
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PMID:Allopurinol promotes and butylated hydroxy toluene prevents sugar-induced cataractogenesis. 234 94

Previous evidence has shown clearly that sugar cataract formation results from unusually high intracellular levels of polyol. Documentation of polyol-related histological changes in the cortical fiber cells of the equatorial zone has been extensive. However, little attention has been given to the early changes in the lens epithelial cells, in spite of the fact that the highest level of aldose reductase is found in this layer of the lens. Also, cultured lens epithelial cells exposed to high sugar levels exhibit rapid accumulation of polyol and show ultrastructural alterations. Therefore, a study was designed to evaluate the role of the lens epithelium in sugar cataract formation. Specifically, an attempt was made to localize the earliest fine structural lesions in intact lenses of galactose-fed rats and to test their relation to aldose reductase. Rats were fed either a normal diet or a 50% galactose diet with or without sorbinil, an aldose reductase inhibitor. Rats were killed at varying periods of time ranging from 6 to 96 hr, and the eyes were processed for light and electron microscopy. The first detectable abnormalities occurred after 36 hr of galactose feeding, and were limited to the central lens epithelium. Cell edema, apparent dilution of cytoplasm, rounding of nuclei, aberrant intracellular vacuoles, and loss of normal tortuosity of cell boundaries were the salient lesions. No changes were detectable in the equatorial zone until 48 hr, and no deviation from the control structure was found in any of the rats treated with an aldose reductase inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of lens epithelium in sugar cataract formation. 237 60

Soluble lens crystallins from 6-10-week-old, galactose-fed, male Sprague-Dawley rats were analyzed by two-dimensional polyacrylamide gel electrophoresis at each of the five Sippel stages of cataractogenesis. Electrophoretograms were compared with similarly analyzed crystallins from comparably aged, chow-fed controls. Polypeptides were assigned to crystallin families and subfamilies on the basis of chromatographic fractionations with Sephadex G-200, superfine. Staining intensities of polypeptides from control lenses remained essentially unchanged throughout the experimental period, while those of the polypeptides from cataractous lenses showed non-uniform changes. Staining of the genomic gamma-crystallins increases up to at least stage 3; by stage 4, staining of gamma-chains, with perhaps those of gamma 5 and gamma 6 excepted, diminishes and in the total cataract, staining of all chains is further reduced. With possibly the addition of one chain, the total number of postsynthetically modified gamma-crystallins in cataractous lenses does not exceed that in the comparably aged normal lens. The genomic alpha- and beta-crystallin polypeptides are sustained close to normal levels up to stages 3 or 2, respectively, after which their gradually falling levels are accompanied by the generation of new species or elevated levels of existing post-translational species. An exception to this behavior is the rapid and total loss of beta B1a, a genomic subunit implicated in the aggregation of beta H-crystallins. Charge heterogeneity and variable pI displayed by beta B1a and other highly cationic beta- and gamma-crystallin polypeptides can be induced during isoelectric focusing and may be due to thiol group oxidation.
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PMID:Differential effects of galactose-induced cataractogenesis on the soluble crystallins of rat lens. 237 84

Previous work from this laboratory has suggested that swollen nucleated fiber cells can survive in mature galactose-cataracts. Evidence for this observation was derived from analysis on the in vitro translation products of mRNA isolated from normal lens and lens undergoing development of galactose-cataracts. Additional studies on the abundance of a fiber cell specific gene product (MP26 mRNA) in both normal and cataractous lens mapped out gene response to: (1) differentiation of epithelial cells to fiber cells, (2) levels of this differential gene activity and its anatomical location in initiation and maturation of galactose-cataracts, and (3) distribution of MP26 mRNA in fibers of normal and cataractous lens. The results from these studies demonstrated that mRNA subsistence in lens undergoing osmotic cataract development might be an indication of occurrence of mechanisms responsible for the reversibility of that type of cataracts. Presumably, reversibility requires propagation and maintenance of the total population of lens specific mRNAs, as our data suggests.
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PMID:Messenger RNA population in normal and cataractous rat lens. A minireview. 248 80

The purpose of this overview is to promote an interest in understanding and reducing the possible occupational health risks of microwave radiation on the eye. Microwaves act on living tissue through two types of mechanisms, thermal and nonthermal. Lens opacities can be induced in experimental animals at relatively high intensities (power densities greater than 100 mW/cm2). For lower intensities, lens changes may depend on the cumulative dose. At "nonthermal intensities", microwaves can act as a trigger and set off changes in the living tissues (e.g. Ca++ efflux). Some cataract-causing agents (alloxan and galactose) act synergistically with microwaves. Microwaves also accelerate formation of cataracts due to diabetes. The corneal endothelium can be damaged by microwaves alone or in combination with some drugs. Microwave degeneration of retinal nerve endings and a small increase in retinal permeability were also found in animals. The effect of long-term low-intensity microwave exposure on the human lens remains poorly understood. Several reports have implicated occupational microwave exposure as a factor in increasing the rate of lens aging and retinal injury in microwave workers. In Canada, recommended microwave exposure limits are set at 25 mW/cm2 for microwave workers and at 1 mW/cm2 for the general public (both averaged over 1 minute). The Australian microwave exposure safety standard (1985) recommends pre- and post-employment eye examinations for workers.
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PMID:Effects of microwave radiation on the eye: the occupational health perspective. 248 31


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