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)

Macular edema has been observed frequently in man after cataract extraction, but pathogenic mechanisms remain unclear. Seven eyes of four young adult rhesus monkeys underwent lens extraction. The retinas and maculae of these eyes were examined by ophthalmoscopy fundus photography, fluorescein angiography, light and electron microscopy, and the horseradish peroxidase tracer technique. In the macular region, the blood-retinal barrier at the retinal vasculature was disrupted in three of the seven eyes. All three eyes had had vitreous loss during lens extraction. Horseradish peroxidase was observed both intracellularly and extracellularly in the maculae. In contrast, the blood-retinal barrier at both the retinal pigment epithelium and the retinal vasculature of the peripheral retina in most eyes was intact. We conclude that macular edema secondary to lens extraction is due to disruption of the blood-retinal barrier at the levels of the retinal vasculature and the retinal pigment epithelium.
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PMID:Experimental macular edema after lens extraction. 40 67

The capacity of myeloperoxidase which is the product of polymorphonuclear leucocytes to induce the lens opacity was studied in young and old rabbits. It was found that the injection of myeloperoxidase solution into anterior chamber of the eye causes the irreversible lens opacification in old rabbits, not in young ones. Light microscopy of the lens section has shown the following alterations: the local thickening of the anterior capsule, disorderly accumulation of epithelial cells, formation of so-called "bladder cells" under the lens epithelium. Changes in experimental eyes are typical for cataract.
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PMID:[The role of myeloperoxidase, a product of the polymorphonuclear leukocytes, in the pathogenesis of cataract]. 133 3

Lens permeability has been shown to be compromised during galactose-induced cataract development in rats. Recent studies have demonstrated permeability and diffusion pathways as well as endocytotic activity in normal lenses of different species using tracers of different molecular weights. We investigated the permeability and diffusion of tracers in normal rat lenses and in lenses during cataract development using three different molecular weight tracers, lanthanum nitrate (LN, MW 430), ruthenium red (RR, MW 858.5) and horseradish peroxidase (HRP, MW 40.000) for this study. Sprague Dawley rats weighing 50gms were fed Purina Rat Chow with or without galactose. Our results, based on transmission electron microscopy, show that all tracers penetrated through the capsule and the basal portion of the intercellular spaces. While the diffusion of RR was restricted to the epithelial cell layer, LN and HRP were observed in intercellular spaces in cortical fiber cells. In the HRP "washout" studies, HRP could be readily removed from the intercellular spaces in the basal region in the epithelial cell layer. This and other observations suggest the presence of a barrier (tight-junction) in the apical region. Our studies also suggest an influx of tracers in the lens, specifically LN and HRP, through the equatorial region. The permeability of the tracers increased and endocytotic vesicles with tracers were often found associated with the lateral and basal membranes of epithelial cells in the galactose-fed rats at the precataractous and mature cataractous stages. This study provides further support for the presence of a tight-junction between epithelial cells and indicates the movement of tracers through the equatorial region. Moreover, it confirms previous observations that indicated alterations in lens permeability during galactose cataractogenesis.
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PMID:Alterations in lens permeability during galactose cataract development in rat. 137 37

Nuclear cataract formed in rat lens in response to a protocol of multiple, low doses of sodium selenite. Nuclear cataract occurred, in both Wistar and Sprague-Dawley rats, following five subcutaneous injections of selenite over an 8-day period with an accumulated dose of 40-50 nmol selenite g-1 body weight. Glutathione content decreased within the first 24 hr of treatment and remained at 60% of controls. Lipid peroxidation occurred in Wistar rats prior to nuclear cataract formation. A two to three-fold increase in calcium concentration and decreased protein content accompanied nuclear cataract development. Enzyme activities were measured for glutathione peroxidase, glutathione reductase, and glutathione S-transferase, and only the peroxidase activity remained constant through the period of cataract formation. This protocol resulted in nuclear cataracts similar in appearance to those observed with a single, acute dose of selenite. The opportunity to control the rate of selenite-dependent cataract formation allows further definition of precataractous events.
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PMID:Biochemical changes and cataract formation in lenses from rats receiving multiple, low doses of sodium selenite. 147 77

The ability of transparent and cataractous human, rabbit and mice lenses to metabolize hydrogen peroxide in the surrounding medium was evaluated. Using a chemiluminescence method in a system of luminol-horseradish peroxidase and a photometric technique, the temperature-dependent kinetics of H2O2 decomposition by lenses were measured. The ability of opaque human lenses to catalyze the decomposition of 10(-4) M H2O2 was significantly decreased. However, this was reversed by the addition of GSH to the incubation medium. Incubation of the mice lenses with the initial concentration H2O2 10(-4) M led to partial depletion of GSH in normal and cataractous lenses. Human cataractous lenses showed decreased activities of glutathione reductase, glutathione peroxidase (catalyzing reduction of organic hydroperoxides including hydroperoxides of lipids), superoxide dismutase, but no signs of depletion in activities of catalase or glutathione peroxidase (utilizing H2O2). The findings indicated an impairment in peroxide metabolism of the mature cataractous lenses compared to normal lenses to be resulted from a deficiency of GSH. An oxidative stress induced by accumulation of lipid peroxidation products in the lens membranes during cataract progression could be considered as a primary cause of GSH deficiency and disturbance of the redox balance in the lens.
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PMID:Peroxide-metabolizing systems of the crystalline lens. 173 65

Altered permeability of the iris vessels of monkey eyes following extra-capsular cataract extraction and posterior chamber intraocular lens implantation was studied by transmission electron microscopy using horseradish peroxidase (HRP) as a tracer. In control animals, HRP-reaction products were confined to the vascular lumens and to a small number of vesicles on the luminal side of the endothelial cells. In experimental animals, however, the interendothelial junctions of the iris vessels were filled with HRP-reaction products, and the endothelial cells of the iris vessels contained a large number of HRP-labeled plasmalemmal vesicles that opened into the basal lamina. HRP-reaction products were also found in the surrounding iris stroma of these experimental animals.
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PMID:Altered permeability of iris vessels following posterior chamber lens implantation: an electron microscopic study. 177 Jun 76

Lens antioxidative enzyme activity (catalase, superoxide dismutase, glutathione peroxidase) in cataract as well as the possibility of cataract induction by the lipid peroxidation products and their influence on the content of reduced thiols (oxy-red balance) were studied. It was shown that the rate of the H2O2 decomposition by the human cataract lenses is lowered in comparison with the normal lenses. This is not due to the lowered catalase or glutathione-peroxidase 1 activity, but depends on the deficiency of reduced glutathione in the lens. Activity of superoxide dismutase and glutathione peroxidase metabolizing organic hydroperoxides is significantly lowered in the cataract lenses. Lipid peroxidation products injected into the rabbit vitreous induce posterior subcapsular cataract, which is accompanied by depletion of reduced glutathione level in the lens. The conclusion is made that two interrelated processes: accumulation of H2O2 and of lipid peroxides induce aggregation of the soluble proteins and the fragmentation of the membrane structures in cataract lenses.
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PMID:[Antioxidative enzyme activity and metabolism of peroxide compounds in the crystalline lens during cataractogenesis]. 381 88

Caffeic acid phenethyl ester (CAPE) was isolated from propolis (a product of honeybee hives) that has been used in folk medicine as a potent antiinflammatory agent. CAPE is cytotoxic to tumor and virally transformed but not to normal cells. Our main goal was to establish whether CAPE inhibits the tumor promoter (12-O-tetradecanoylphorbol-13-acetate)-induced processes associated with carcinogenesis. Topical treatment of SENCAR mice with very low doses (0.1-6.5 nmol/topical treatment) of CAPE strongly inhibits the following 12-O-tetradecanoylphorbol-13-acetate-mediated oxidative processes that are considered essential for tumor promotion: (a) polymorphonuclear leukocyte infiltration into mouse skin and ears, as quantified by myeloperoxidase activity; (b) hydrogen peroxide (H2O2) production; and (c) formation of oxidized bases in epidermal DNA, as measured by 5-hydroxymethyluracil and 8-hydroxylguanine. A 0.5-nmol dose of CAPE suppresses the oxidative burst of human polymorphonuclear leukocytes by 50%. At higher doses (1-10 mumol), CAPE inhibits edema and ornithine decarboxylase induction in CD-1 and SENCAR mice. Interestingly, we discovered that 12-O-tetradecanoylphorbol-13-acetate-induced H2O2 production in bovine lenses also is inhibited by CAPE. Cumulatively, these findings point to CAPE as being a potent chemopreventive agent, which may be useful in combating diseases with strong inflammatory and/or oxidative stress components, i.e., various types of cancer and possibly cataract development.
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PMID:Inhibition of tumor promoter-mediated processes in mouse skin and bovine lens by caffeic acid phenethyl ester. 768 Feb 81

Lipid peroxidation (LPO) could be one of the mechanisms of cataractogenesis, initiated by enhanced production of oxygen free radicals in the eye fluids and tissues and impaired enzymatic and non-enzymatic defences of the lens. The increased concentrations of primary molecular LPO products (diene conjugates, lipid hydroperoxides) and end fluorescent LPO products were detected in the lipid moiety of the aqueous humor samples obtained from patients with cataract as compared to normal donors. Isolated human transparent and cataractous lenses and normal mouse and rabbit lenses were incubated with liposomes in organ culture in the presence and absence of LPO inhibitors, free radical scavengers and enzymes (catalase, superoxide dismutase (SOD)) in order to examine the potential of the lenses to induce LPO in the surrounding medium. LPO assayed spectrophotometrically were diene and triene conjugates, and malonaldehydes (MDA) were determined as thiobarbituric acid-reactive material. A chemiluminescence detection catalysed by peroxidase was used to measure H2O2 and O2-. was assayed spectrophotometrically using cytochrome C reduction. The level of lipid peroxides in liposomes was significantly (2.5-4.5-fold) higher after 3 h of incubation of the transparent lenses (or the lenses at the initial stage of cataract) than after the proper time of incubation of human mature cataractous lenses and virtually no oxidation of liposomes was detected in the absence of the lens. LPO in this system was decreased in the presence of free radical scavengers and enzymes that degrade H2O2 (EDTA, SOD, L-carnosine, chelated iron and catalase). The most effective agent was EDTA which chelates the free metal cations required to generate O2-. radicals that initiate the free radical process culminating in LPO. Lenses generated more H2O2 into the medium in the presence of exogenous ascorbate. Release of the oxidants, (O2-., H2O2, OH. and lipid hydroperoxides) by the intact lenses in the absence of respiratory inhibitors indicates that these metabolites are normal physiological products inversely related to the lens life-span potential (maturity of cataract) generated, probably, through the metal-ion catalysed redox-coupled pro-oxidant activation of the lens reductants (ascorbic acid, glutathione).
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PMID:Lipid peroxide and reactive oxygen species generating systems of the crystalline lens. 831 81

Selenium (Sc) is a trace element which incorporates into the selenoenzyme glutathion peroxidase. Cataractogenesis may be caused either by the excess or deficiency of this trace element. More recently, its potential of becoming a possible environmental pollutant has been emphasized. In an attempt to reveal the relationship of this element with cataractogenesis, we detected its level in 48 serum, 36 lens and 9 aqueous humour samples of 48 patients with senile cataract, comparing the results with appropriate controls. Selenium levels (mean +/- SD) of cataractous patients were found to be 0.28 +/- 0.04 microgram/ml (CI: 0.27 to 0.29 microgram/ml) in sera (controls: 0.32 +/- 0.04 microgram/ml; CI: 0.30 to 0.34 microgram/ml, p < 0.0001), 5.43 +/- 3.07 microgram/g dry weight (CI: 4.43 to 6.43 microgram/g dry weight) in lens (controls: 4.43 +/-2.53 microgram/g dry weight; CI: 2.78 to 6.08 microgram/g dry weight; p=0.374) and 0.19 +/- 0.06 microgram/ml (CI:0.15 to 0.23 microgram/ml) in aqueous humour samples (controls: 0.31 +/-0.12 microgram/ml; CI: 0.24 to 0.38 microgram/ml, p = 0.02). When patient subgroups were analyzed, serum Se levels were found to be 0.28 +/- 0.05 microgram/ml (CI: 0.26 to 0.30 microgram/ml in the nuclear cataract and 0.28 +/- 0.02 microgram/ml (CI: 0.27 to 0.30 microgram/ml) in the cortical cataract. Lens Se levels, on the other hand, were detected as 5.91 +/- 3.56 microgram/g dry weight (CI:4.49 to 7.33 microgram/g dry weight) in the nuclear cataract and 4.47 +/- 1.40 microgram/g dry weight (CI: 3.68 to 5.26 microgram/g dry weight) in the cortical cataract. It is anticipated that decreased Se in aqueous humour and sera of patients with senile cataract may reflect defective antioxidative defense systems which may lead to the formation of cataract.
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PMID:Selenium concentrations in serum, lens and aqueous humour of patients with senile cataract. 864 78


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