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

The role of nutritional supplementation in prevention of onset or progression of ocular disease is of interest to health care professionals and patients. The aim of this review is to identify those antioxidants most appropriate for inclusion in an ideal ocular nutritional supplement, suitable for those with a family history of glaucoma, cataract, or age-related macular disease, or lifestyle factors predisposing onset of these conditions, such as smoking, poor nutritional status, or high levels of sunlight exposure. It would also be suitable for those with early stages of age-related ocular disease. Literature searches were carried out on Web of Science and PubMed for articles relating to the use of nutrients in ocular disease. Those highlighted for possible inclusion were vitamins A, B, C and E, carotenoids beta-carotene, lutein, and zeaxanthin, minerals selenium and zinc, and the herb, Ginkgo biloba. Conflicting evidence is presented for vitamins A and E in prevention of ocular disease; these vitamins have roles in the production of rhodopsin and prevention of lipid peroxidation respectively. B vitamins have been linked with a reduced risk of cataract and studies have provided evidence supporting a protective role of vitamin C in cataract prevention. Beta-carotene is active in the prevention of free radical formation, but has been linked with an increased risk of lung cancer in smokers. Improvements in visual function in patients with age-related macular disease have been noted with lutein and zeaxanthin supplementation. Selenium has been linked with a reduced risk of cataract and activates the antioxidant enzyme glutathione peroxidase, protecting cell membranes from oxidative damage while zinc, although an essential component of antioxidant enzymes, has been highlighted for risk of adverse effects. As well as reducing platelet aggregation and increasing vasodilation, Gingko biloba has been linked with improvements in pre-existing field damage in some patients with normal tension glaucoma. We advocate that vitamins C and E, and lutein/zeaxanthin should be included in our theoretically ideal ocular nutritional supplement.
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PMID:An ideal ocular nutritional supplement? 1522 13

Wistar rat pups treated with curcumin, a natural constituent of Curcuma longa before being administered with selenium showed no opacities in the lens. The lipid peroxidation, xanthine oxidase enzyme levels in the lenses of curcumin and selenium co-treated animals were significantly less when compared to selenium treated animals. The superoxidase dismutase and catalase enzyme activities of curcumin and selenium co-treated animal lenses showed an enhancement. Curcumin co-treatment seems to prevent oxidative damage and found to delay the development of cataract.
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PMID:Antioxidant effect of curcumin in selenium induced cataract of Wistar rats. 1526 Jan 12

Selenium biochemistry is reviewed in respect to its presumed relevance to age-related ocular diseases. Selenium is an essential trace element that exerts its physiological role as selenocysteine residue in at least 25 distinct selenoenzymes in mammals. Lack of GPx-1 due to alimentary selenium deprivation has been inferred to induce cataract in rats and was demonstrated to cause cataracts in mice by targeted gene disruption. The role of other selenoproteins in the eye remains to be worked out. Selenium in excess of the tiny amounts required for selenoprotein synthesis is toxic in general and causes cataracts in experimental animals. Clinical evidence for a protective role of selenium in the development of cataract, macula degeneration, retinitis pigmentosa or any other ocular disease is not available, likely because suboptimum selenium intake, as it may result from unbalanced diet, does not cause any pathologically relevant selenium deficiency in the eye. At present, there is neither theoretical nor an empirical basis to expect beneficial effects of selenium supplementation beyond the dietary reference intakes of 55 microg/day in the context of ocular diseases.
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PMID:Selenium, selenoproteins and vision. 1560 19

The objective of this study was to determine the prevalence of age-related cataract in high-selenium areas of China. This is a cross-sectional study of 1,522 persons aged 50 years and more who were selected as a representative sample from the Enshi prefecture in Hubei province. All lenses were graded and classified for opacities by slit lamp after papillary dilation, using the Lens Opacification Classification System II. The age-related cataract patients were 418 cases (33.28%). The prevalence of age-related cataract was 37.2% in women and 26.0% in men. The prevalence of nuclear cataract was 23.7%; cortical cataract was 22.4% and posterior subcapsule cataract was 5.2%. The prevalence of cataract of the 50-59 group was 13.41%; 60-69 group was 42.15%; 70 and over group was 61.9%. The prevalence of age-related cataract in high-selenium areas has not significantly increased; to some extent, the high selenium intake will not become a risk factor for the increase of cataract incidence.
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PMID:Prevalence of age-related cataract in high-selenium areas of China. 1897 73

The aim of this study was to investigate whether curcumin and aminoguanidine (AG) prevent selenium-induced cataractogenesis in vitro. On postpartum day 8, transparent isolated lens were incubated in 24 well plates containing Dulbecco's Modified Eagle Medium (DMEM). Isolated lens of group I were incubated with DMEM medium alone. Group II: lenses incubated in DMEM containing 100microM sodium selenite; group III: lenses incubated in DMEM containing 100microM sodium selenite and 100microM curcumin; group IV: lenses incubated in DMEM containing 100microM sodium selenite and 200microM curcumin; group V: lenses incubated in DMEM containing 100microM sodium selenite and 100microM AG; group V: lenses incubated in DMEM containing 100microM sodium selenite and 200microM AG. On day 12, cataract development was graded using an inverted microscope and the lenses were analyzed for enzymic as well as non-enzymic antioxidants, lipid peroxidation (LPO), nitric oxide (NO), superoxide anion (O(2)(-)) and hydroxyl radical generation (OH) and inducible nitric oxide synthase (iNOS) activity by Western blotting and RT-PCR. All control lenses in group I were clear (0). In groups II and III, all isolated lenses developed cataract with variation in levels (+++ or ++), whereas isolated lenses from groups IV, V and VI were clear (0). In agreement to this, a decrease in antioxidants and increased free radical generation and also iNOS expression were observed in selenium exposed lenses when compared to other groups. AG (100microM) was found to be more effective in anti-cataractogenic effect than curcumin (200microM). Curcumin and AG suppressed selenium-induced oxidative stress and cataract formation in isolated lens from Wistar rat pups, possibly by inhibiting depletion of enzymic as well as non-enzymic antioxidants, and preventing uncontrolled generation of free radicals and also by inhibiting iNOS expression. Our results implicate a major role for curcumin and AG in preventing cataractogenesis in selenite-exposed lenses, wherein AG was found to be more potent.
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PMID:Anti-cataractogenic effect of curcumin and aminoguanidine against selenium-induced oxidative stress in the eye lens of Wistar rat pups: An in vitro study using isolated lens. 1948 Oct 68

The generation of free radicals has been implicated in the causation of cataract, and compounds that can scavenge free radicals ameliorate the disease process. This study investigated the possible free radical scavenging potential of curcumin at a dose of 75 mg/kg body wt on selenium-induced cataract in rat pups. Intraperitoneal injection of sodium selenite (15 micromol/kg body wt) into 8- to 10-day-old rat pups led to severe oxidative stress in the eye lens as evidenced by increased nitric oxide, superoxide anion, and hydroxyl radical generation and inducible nitric oxide synthase expression that probably led to cataract formation. Selenium exposure also caused an increase in total calcium in the eye lens and significantly inhibited the activity of Ca(2+) ATPase but not Na(+)/K(+) ATPase or Mg(2+) ATPase. On the other hand, pretreatment with curcumin, but not simultaneous or posttreatment, led to a decrease in oxidative stress and also rescued the selenium-mediated increase in lens Ca(2+) and inhibition of Ca(2+) ATPase activity in the eye lens. The results of this study demonstrate that an increase in free radical generation triggered by selenium could cause inactivation of lens Ca(2+) ATPase leading to Ca(2+) accumulation. This enhanced Ca(2+) can cause activation of calpain-mediated proteolysis in the lens, resulting in lens opacification. Curcumin in this study was able to prevent selenium-induced oxidative stress leading to activation of Ca(2+) ATPase and inhibition of lens opacification. Thus, curcumin has the potential to function as an anticataractogenic agent, possibly by preventing free radical-mediated accumulation of Ca(2+) in the eye lens.
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PMID:Curcumin prevents free radical-mediated cataractogenesis through modulations in lens calcium. 1993 68

Recently, much interest has been generated in the search for phytochemical therapeutics, as they are largely free from adverse side effects and economical. The goal of this study was to determine the efficacy of Vitex negundo in modulating the selenite-induced oxidative stress in vivo model. Sprague-Dawley rat pups of 8 days old were used for the study and divided into control (G I), selenite induced (G II), and selenite + V. negundo treated (G III). Cataract was induced by the single subcutaneous injection of sodium selenite (4 mg/kg body weight) on the tenth day and V. negundo (2.5 mg/Kg body weight) administered intraperitoneally from eighth to 15th day. Morphological examination of the rat lenses revealed no opacification in G I and mild opacification in G III whereas dense opacification in G II (stages 4-6). Levels of selenium in G II and G III showed no significant changes. The activities of superoxide dismutase, catalase, and Ca(2+)ATPase were significantly increased in G III compared to G II (p < 0.05), while lower level of reactive oxygen species, Ca(2+), and thiobarbituric acid reactive substances were observed in G III compared G II (p < 0.05). These results indicate the therapeutic potential of methanolic extract of V. negundo on modulating biochemical parameters against selenite-induced cataract, which have been reported in this paper for the first time.
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PMID:Vitex negundo modulates selenite-induced opacification and cataractogensis in rat pups. 2017 76

Selenium is an essential mineral and severe selenium deficiency is known to cause significant health problems. It has been well documented that New Zealand soil is low in selenium. Recent studies have addressed the roles of selenoproteins in the eyes, with evidence suggesting that selenium supplementation may have a role in preventing cataract formation and age-related maculopathy. This paper summarises the role of selenium in ocular and general health and discusses selenium supplementation in a New Zealand specific context.
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PMID:Selenium and ocular health in New Zealand. 2064 2

Cataract, the opacification of eye lens, is the leading cause of blindness worldwide. At present, the only remedy is surgical removal of the cataractous lens and substitution with a lens made of synthetic polymers. However, besides significant costs of operation and possible complications, an artificial lens just does not have the overall optical qualities of a normal one. Hence it remains a significant public health problem, and biochemical solutions or pharmacological interventions that will maintain the transparency of the lens are highly required. Naturally, there is a persistent demand for suitable biological models. The ocular lens would appear to be an ideal organ for maintaining culture conditions because of lacking blood vessels and nerves. The lens in vivo obtains its nutrients and eliminates waste products via diffusion with the surrounding fluids. Lens opacification observed in vivo can be mimicked in vitro by addition of the cataractogenic agent sodium selenite (Na(2)SeO(3)) to the culture medium. Moreover, since an overdose of sodium selenite induces also cataract in young rats, it became an extremely rapid and convenient model of nuclear cataract in vivo. The main focus of this review will be on selenium (Se) and its salt sodium selenite, their toxicological characteristics and safety data in relevance of modelling cataractogenesis, either under in vivo or in vitro conditions. The studies revealing the mechanisms of lens opacification induced by selenite are highlighted, the representatives from screening for potential anti-cataract agents are listed.
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PMID:Different experimental approaches in modelling cataractogenesis: An overview of selenite-induced nuclear cataract in rats. 2121 65

The 15-kDa selenoprotein (Sep15) is a thioredoxin-like, endoplasmic reticulum-resident protein involved in the quality control of glycoprotein folding through its interaction with UDP-glucose:glycoprotein glucosyltransferase. Expression of Sep15 is regulated by dietary selenium and the unfolded protein response, but its specific function is not known. In this study, we developed and characterized Sep15 KO mice by targeted removal of exon 2 of the Sep15 gene coding for the cysteine-rich UDP-glucose:glycoprotein glucosyltransferase-binding domain. These KO mice synthesized a mutant mRNA, but the shortened protein product could be detected neither in tissues nor in Sep15 KO embryonic fibroblasts. Sep15 KO mice were viable and fertile, showed normal brain morphology, and did not activate endoplasmic reticulum stress pathways. However, parameters of oxidative stress were elevated in the livers of these mice. We found that Sep15 mRNA was enriched during lens development. Further phenotypic characterization of Sep15 KO mice revealed a prominent nuclear cataract that developed at an early age. These cataracts did not appear to be associated with severe oxidative stress or glucose dysregulation. We suggest that the cataracts resulted from an improper folding status of lens proteins caused by Sep15 deficiency.
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PMID:Roles of the 15-kDa selenoprotein (Sep15) in redox homeostasis and cataract development revealed by the analysis of Sep 15 knockout mice. 2176 92


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