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)

The clinical and electro-neurographic examinations were carried out in 54 patients aged 21-67 years (mean = 41.8) with IDDM of at least 10-year duration, and 25 subjects aged 19-62 years (mean = 39.0) as a control group. The aim of the study was the determination of: 1) the frequency of polyneuropathy appearance in patients with IDDM of at least 10-year duration; 2) the usefulness of electroneurography for detection of subclinical impairment of peripheral nervous system in diabetics; 3) the characterization of electro-neurographic abnormalities in diabetic neuropathy; 4) the influence of diabetes duration and metabolic control on severity of peripheral nerves affection; 5) the relationship between polyneuropathy and retinopathy, nephropathy and cataract occurrence in diabetic patients. Polyneuropathy was diagnosed--clinically in 67% of patients, electro-neurographically in 85% of patients. The neurographic study proved high sensitivity for detection of subclinical affection of peripheral nerves in diabetics. The electro-neurographic abnormalities appeared more frequently and were more considerable in the group of patients with clinical polyneuropathy. Frequency of the sensory and motor nerve fibres involvement was similar. The electroneurographical abnormalities corresponded with the features of mixed--axonal and demyelinating type of neuropathy. It was disclosed that the degree of neurographical changes did not depend on duration and severity of hyperglycemia in late period of the disease. A moderate relationship between occurrence of polyneuropathy and retinopathy, nephropathy as well as diabetic cataract was revealed.
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PMID:[Clinical and electroneurographic changes in the peripheral nervous system of patients with chronic insulin-dependent diabetes (IDDM)]. 750 45

The etiology of diabetic cataract is usually explained by the following process; the conversion of glucose and galactose to polyol by aldose reductase, then the accumulation of polyol in lens, and the opacity of lens. Another explanation is that the hyperoxidation of lens membrane due to an increase of active oxygen and lipid peroxide in lens induces diabetic cataract. The experimental animals used in the present study were rats with galactose cataract and streptozotocin cataract. We measured the levels of antioxidants (glutathione, ascorbic acid) and lipid peroxide (malonodialdehyde) in lens, aqueous humor and vitreous body. Furthermore we studied the effects of aldose reductase inhibitor (TAT) on these levels. In streptozotocin diabetes rats, the increased malonodialdehyde levels in lens, aqueous humor and serum were suppressed by TAT administration. In galactose and streptozotocin diabetes rats, the decreased levels of glutathione and ascorbic acid were suppressed by TAT administration.
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PMID:[Biochemical changes in lens, aqueous humor and vitreous body and effects of aldose reductase inhibitor (TAT) on rats with experimental diabetes]. 755 22

To evaluate accumulation of advanced glycation end-products (AGE) in diabetes and its possible correlation with late diabetic complications, AGE levels were measured by spectrofluorimetry in eye lens and sciatic nerve proteins and isolated tail tendon collagen of rats with experimental diabetes of 3- and 6-month duration. The values obtained were compared to those from age-matched control rats and correlated with cataract presence and somatosensory evoked potential (SEP) alterations. Diabetic animals had increased AGE levels in all tissues at both times; cataract developed in 29% of diabetic rats at 3 months and in 57% at 6 months; SEP conduction velocity was reduced in diabetic animals both at 3 (54.5 +/- 1.8 S.E.M. m/s vs. 73.9 +/- 1.0, P < 0.0001) and 6 months (59.5 +/- 1.4 vs. 71.5 +/- 1.6, P < 0.0001) from diabetes induction. No eye lens AGE level differences were observed when cataract presence was considered. Interestingly, in diabetic rats, increased sciatic nerve AGE levels were associated with reduced SEP. These data show that: (1) AGE levels are increased as early as 3 months from development of hyperglycemia; (2) other factors, in addition to an enhanced rate of fluorescent AGE formation, might play important roles in the pathogenesis of diabetic cataract; (3) increased peripheral nerve AGE levels are associated with SEP alterations.
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PMID:Role of advanced glycation end-products (AGE) in late diabetic complications. 758 17

This paper reviews the changes which occur in the human lens in diabetes. They include refractive changes and cataract and age-related increases in thickness, curvatures, light scattering, autofluorescence and yellowing. The incidence of cataract is greatly increased over the age of 50 years, slightly more so in women, compared with non-diabetics. Experimental models of sugar cataract provide some evidence for the mechanism of the uncommon, but morphologically distinct, juvenile form of human diabetic cataract, where an osmotic mechanism due to sugar alcohol accumulation has been thoroughly studied in diabetic or galactose-fed rats. The discrepancy between the ready accumulation of sugar alcohol in the lens in model systems and the very slow kinetics of aldose reductase (AR) has not been satisfactorily explained and suggests that the mechanism of polyol formation is not yet fully understood in mammalian systems. The activity of AR in the human lens lies mainly in the epithelium and there appears to be a marginal expectation that sufficient sorbitol accumulates in cortical lens fibres to explain the lens swelling and cataract on an osmotic basis. This is even more so in the cataracts of adult diabetics, which resemble those of age-related non-diabetic cataracts in appearance. The very low levels of sorbitol in adult diabetic lenses make an osmotic mechanism for the increased risk of cataract even less likely. Other mechanisms, including glycation and oxidative stress, are discussed. The occurrence of cataract is a predictor for increased mortality in the diabetic.
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PMID:The lens in diabetes. 760 46

There are two approaches to the question of whether solar radiation contributes to human cataract. The first, epidemiological studies, investigates correlations between man's environmental UV dose and cataract frequency. The second, animal models, investigates the effects of varying UV strengths and spectra on lens opacification in vivo or in vitro. While the latter approach typically provides for direct evidence, the data must still be extrapolated to human lenses. Results of physiological studies suggest that UV photons interact with proteins of the epithelial cell membranes, in particular tryptophan residues, transport ATPases and cytoskeletal proteins. One hypothesis is that damage to ion pumps and channels accumulates over the years as repair processes incompletely restore membrane function. Peroxidative damage is likely in view of the formation of UV-induced lipid peroxides in the lens epithelial membranes. Loss of homeostatic control of ions, particularly Ca++, leads to crystallin disorder in small regions of the underlying fiber cells. In our diabetic cataract studies, intracellular Ca++ electrodes detected large shifts in intracellular Ca++ before bulk-lens changes were apparent. Similar occurrences likely characterize UV cataract. Our lab is one of few studying lens physiology and how it is altered following transient exposures to UV-B and UV-A, both of which pass through the cornea. Some changes include: loss of epithelial cell GSH; elevated Ca++; loss of membrane voltage; impaired transport of Na+; increased permeability to ions and water; inhibition of critical enzymes; and a decrease in the rate of membrane synthesis.
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PMID:A review of the evidence that ultraviolet irradiation is a risk factor in cataractogenesis. 763 90

Experimental work in our laboratory has confirmed the protective activity of vanadium compounds on hyperglycemia and glycosuria in streptozotocin (STZ) diabetes. Furthermore, diabetic cataract has also been partially prevented. Nevertheless, the combination of a natural antioxidant, vitamin E, with Na3 VO4 has not further enhanced this ameliorating effect. Our experimental approach has been an attempt to block the prooxidant activity of both STZ and vanadate, with the purpose of eliciting the best possible antidiabetic protection. More recently, a lipid soluble synthetic antioxidant U-78517F, a 2-methylaminochroman, has been reported to have a significant protective effect against brain injury and ischemia. This compound inhibits the iron-dependent lipid peroxidation 100 times more effectively than vitamin E. This investigation has introduced a combination of the vanadium compound plus the aforesaid lazaroid, as its (-) enantiomer, U-83836E, in order to improve the insufficient protection when vitamin E was used. For twelve weeks, male Wistar rats, rendered diabetic with STZ, were administered Na3VO4 in drinking water along with the lazaroid carried by the food. Four, eight and twelve weeks after the beginning of the protective treatment, fluid and food intake, diuresis and excreted feces, glycosuria and proteinuria were determined on biological samples obtained in metabolic cages; body weight and glycemia were also recorded. At weeks 6 and 12 of the treatment, the opaqueness of the eye lenses was controlled and registered. At the end of the experiment, circulating glycosylated hemoglobin (HbA1c), fructosamine, N-acetyl-beta-D-glucosaminidase (NAG), and fluorescent peroxides were evaluated. Within the first month of treatment, protection by the combination paralleled that elicited by vanadate alone. At subsequent steps, U-83836E significantly improved the protective effect of vanadate alone on polydipsia and polyuria, but especially on hyperglycemia and glycosuria. The further ameliorating effect of the lazaroid was also observed on HbA1c and NAG, and, most important, on the cataract. In conclusion, these findings demonstrate that the lazaroid U-83836E succeeds in further protecting the most important symptoms of diabetes treated with vanadate, and that this antioxidant acts effectively even when it is administered orally in food, in a non invasive manner.
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PMID:Amelioration of diabetes and cataract by Na3VO4 plus U-83836E in streptozotocin treated rats. 782 6

Research into the biological basis of lens transparency has demonstrated the implication of lens sugar stress in the diabetic cataract whereas senile cataract is the result of natural degeneration which is enhanced by various external factors such as cosmic and ionizing rays, or oxidative processes. Drugs have been developed which are aimed at being effective on lens pathological physiology and metabolism, concurrently. Such molecules: aldose reductase inhibitors (ARIs: sorbinil, AD-5467, CT-112 and imirestat), acetyl salicylic acid (ASA), salicylate (SA) and sodium monomethyl trisilanol orthohydroxybenzoate (SMB, a prodrug for salicylate) have undergone pharmacodynamic, pharmacokinetic and/or clinical studies which are presented here. ARIs have shown efficacy in slowing down and preventing the progression of experimental sugar cataracts; sorbinil can partially reverse the very early morphological signs of sugar cataract. Sorbinil and imirestat have also demonstrated anti-oxidant properties. ARIs administration (per os or by topical instillation) generally results in lens levels compatible with concentrations that are efficient on biochemical mechanisms of cataract formation. However, at the present time, clinical evaluations are in progress and as yet, there is no confirmation of their efficacy in man. ASA and SA can prevent various mechanisms of lens protein denaturation; they inhibit AR and prevent, in vitro, the formation of some pigments found in the aged cataractous lens. Extrapolation of the ASA ocular pharmacokinetics results in animal to man, suggest that ASA administration per os could result in efficacious levels in the lens. This is also sustained by the observation of a reduced frequency of cataracts in ASA treated diabetic rheumatoid arthritis patients. SMB pharmacokinetic studies have shown small but persistent levels of the active principle in the lens. They suggest that the capsule slows down SA diffusion into the lens and that, on the contrary, lens epithelium facilitates its penetration. Preliminary results of pharmacodynamic studies are given.
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PMID:Drugs designed to maintain the transparence of the ocular lens. 785 38

Lenses of Yellow KK mice with marked obesity and diabetic symptoms were examined by light and electron microscopy. At 2 months of age, the entire lens appeared normal. At 4 months, however, epithelial cells sometimes had become necrotic and showed intranuclear inclusions. At 6 months, the anterior cortical fibers were swollen. At 8 months, the number of intranuclear inclusions of the epithelial cells had increased, and the posterior cortex contained densely stained cells among the fibers, with swollen cytoplasm. At 10 months, these cells had become atrophic. At 12 months, the lens cells in the posterior sutural area showed marked swelling, and the suture was almost separated. This animal model showed a slow progressive cataract in the superficial cortical zone which is similar to the diabetic cataract in human eyes.
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PMID:Histopathological study of congenitally diabetic yellow KK mouse lens. 814 81

Four kinds of lipoproteins contained in human diabetic cataract lens were separated by of sequential flotation in an ultracentrifuge, and the quantities of each were determined by selective precipitation. Chylomicron, very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) were separated from cataract lenses as lipoprotein fractions, and quantified. Chylomicron was present in the largest quantity among the four. There was no significant difference between the total amount of lipoprotein contained in diabetic cataract lenses (96.95 +/- 4.03 micrograms/lens) and that in senile cataract lenses (89.51 +/- 8.35 micrograms/lens). The quantities of VLDL and LDL, however, were significantly larger in diabetic cataract lenses (14.84 +/- 0.55 and 20.97 +/- 0.58 micrograms/lens, respectively) than in senile cataract lenses (6.30 +/- 0.46 and 7.45 +/- 0.61 micrograms/lens, respectively). We demonstrated histologically that LDL receptors are localized on the lens epithelium and its underlying layer.
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PMID:[The lipoproteins in human diabetic cataract]. 819 19

Proton nuclear magnetic resonance (1H-NMR) is one of the most important methods for noninvasively evaluating the state of water in the biological system. It could be useful for evaluation of the early changes of cataract. In this study, in vivo magnetic resonance imaging (MRI) was applied to rat galactosemic cataract, which is a model of the human diabetic cataract, and compared with the histological findings. The relationship between the relaxation times (T1, T2) and the water contents were discussed. The T1 and T2 values were prolonged and the high intensity area of the lens cortex was enlarged from the early stage of the cataract (two days after the intake of galactose). These changes preceded the histological changes. This suggests that MRI is applicable for the evaluation of anti-cataract agents, for example aldose reductase inhibitors, against human diabetic cataract.
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PMID:[Magnetic resonance imaging study on rat sugar cataract]. 825 67


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