DOCSLIB.ORG

TYPES of Cfltfirflct TYPES of CATARACT

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
TYPES of Cfltfirflct TYPES of CATARACT TYPES OF CflTfiRflCT TYPES OF CATARACT 1. Senile Cataract 2. Diabetic Cataract 3. Galactosemic Cataract 4. Xylose Cataract 5. Toxic Cataract 6. Radiation Cataract 7. Nutritional Cataract 8. Traumatic Cataract 9. Cold Cataract 10. Genetic Cataract. 11. Development Cataract Senile Cataract The great majority of human cataracts are senile cataracts. The human lens normally undergoes changes with age : it slowly increases in size as new lens fibers develop throughout life; older lens fibers in the depths of the lens become dehydrated, compacted and "sclerosed", a yellow brown pigment accumulates. The increase in the optical density of the nucleus tends to increase the refractive power of the lens so that less hyperoptic spectacle correction may be needed in old age. The yellow brown pigment may become so dense as to constitute nuclear sclerosis and later brunescent cataract. Cortical cataract, however, is the development of vacuoles and water clefts in the lens cortex that tend to increase in extent and in the advanced state give the lens a pear like appearance. Approximately 60% of human beings have some alterations in lens transparency after 60 years of age. Progression of lens changes differ among individuals and lens opacities can cause visual deficits in a shorter or longer period of time. 22 Diabetic Cataracts Increased levels of glucose in the aqueous and lens are found in patients with diabetes mellitus. In general, the glucose concentration in the aqueous parallels the concentrations in the plasma. From the aqueous, glucose diffuses rapidly into the lens. The lens metabolizes glucose through four main pathways. 1. Anaerobic glycolysis 2. The Hexose Monophosphate shunt 3. Citric Acid Cycle 4. Sorbitol Pathway. Basically the initial rate of glucose metabolism in the lens is determined by hexokinase, a regulatory enzyme. In diabetes excessive glucose in the lens (over 200 mg%) saturates hexokinase. Glucose then piles up and is converted partly into sorbitol and fructose (Kinoshita et al. 1963). NADPH NADP+ Glucose -^ Sorbitol Aldose reductase NAD* ^ Polyol dehydrogenase ATP NADH V Hexokinase Fructose V G6PD Glucose-6-Phosphate ->HMP Shunt i Pyruviru\ c acid LDH LactiIc Acid Aldose reductase catalyzes the glucose to sorbitol reaction. High levels of sorbitol and fructose were found in diabetic animal lenses by Kuck (1961) and in human diabetic lenses by Pirie and Van Heyningen (1964). The excess of sorbitol is also found in rabbit lenses cultured in vitro in high glucose media. (Kinoshita et al, 1963). 23 The effects of excessive sorbitol and fructose in the diabetic lens results in increased hydration and sodium ions gain with subsequent loss of K+ ions, amino acids and inositol (Kinoshita, 65b). The swelling of the lens has led to postulate that high levels of sorbitol in the diabetic lens draw water, thus rupturing lens fibers and causing vacuolation in lens cortex. The rate of cataract progression depends on the glucose levels in serum; the higher the glycemia, the faster the cataracts become mature (Patterson, 1952). In humans, diabetic cataracts are rarely seen in juveniles but may appear suddenly in adults with uncontrolled diabetes mellitus. Other mechanisms beside accumulation of sugar alcohols are also involved in cataract formation in diabetes. The known damage to basement membrane in these patients may be the cause of the decreased fragility of their lens capsule (Caird et al, 1968). Furthermore, excessive red blood cell glycosylation is found in uncontrolled diabetics and it may have an effect on the lens as well. Stevens and coworkers (1978) have found evidence of increased protein glycosylation by animal lenses incubated in high glucose media. The formation of sugar amino acid (lysine) bonds may result in protein aggregation and decreased transparency. 24 Galactosemic Cataract Inability to metabolize galactose occurs in the galactosemias, which may be caused by inherited defects in any of the 3 enzymes marked (1), (2) and (3) as shown below : NADPH NADP+ Galactose -^ Galactitol Aldose reductase ATP Galacto (1) kinase C ADP Galactose-1-P y UDP-Glucose / Galactose-1-P Uridyl V (2) Transferase Glucose 1-P ^ UDP Galactose < •^ UDP Glucose Uridine Diphosphogalactose (3) Excessive galactose in the serum and the lens results in a shift toward the formation of galactitol. The accumulation of galactitol has deleterious effects on the lens and leads to cataract formation. Galactosemic cataract also results due to the excessive amounts of sugar alcohols (Galactitol) drawing water into the lens. Water gains by the lens fibers rupture their membranes, with resultant loss of K*, amino acids and inositol. Xylose Cataract Xylose is the third member of the series of cataractogenic sugars (the others are glucose and galactose). Like other sugar cataracts, Xylitol and Xylulose accumulate in Xylose cataract, but levels are never as high as those of sorbitol and fructose in diabetes. 25 Toxic Cataract Toxic cataract may be defined as lens opacification due to the effects of chemicals upon the lens. These include a number of drugs and poisons which cause cataract. Naphthalene induced experimental cataracts are studied in some more detail. According to van Heyningen and Pirie (1967) Naphthalene is converted into Naphthalene diol. This can be converted in the eye to 1-2 dihydroxynaphthalene which is probably responsible for the blue fluorescene in the eye of the naphthalene-fed rabbit. This is oxidised to beta naphthaquinone (Rees and Pirie, 1967). It reacts with ascorbic acid to form H^O^ which is toxic. One of the early changes is a marked swelling of the lens. An unusual result is thickening of the epithelium to several layers early in the process. Muc" h later (nearly 30 days) when the cataract is mature, the entire capsule is lined with epithelium the cortex is liquefied although the nucleus remains intact. In the postmature stage the epithelium is lost and the fibers fall to pieces within the thickened «apsule. Another suggested mechanism for naphthalene cataract was that based on the finding that one of the elimination products is urinary alpha-naphthyl mercapturic acid. The detoxification of large amounts of naphthalene would theoretically utilize enough cystine to cause a deficiency of this compound. In addition to naphthalene, many other drugs often used therapeutically, at one time, such as dinitrophenol, myeleran and dimethyl sulphoxide, would cause cataracts but not necessarily in man. For example, dimethyl sulphoxide has not reportedly caused any eye damage in man, although it has, in experimental animals, such as dog (Rubin and Bernett, 1967). Radiation Cataract Ionizing radiation (X-rays, gamma rays, neutrons, beta rays) induces lens vacuoles and lens opacities. The lens is affected only by radiation of wavelengths that absorbed. Wavelengths between 293 and 400 mm are transmitted by the cornea and effectively absorbed by the lens, so this is the range of ultraviolet light. 26 potentially most damaging to the lens. Above 1100-1400 m^, the infrared may be injurious, since in this range, the rays are transmitted through the cornea and absorbed by the lens. Radiation affects the permeability of the lens. Lenses exposed to radiation are more leaky to K^ inositol and glutathione. These effects may occur at the level of the membranes of the lens fibers. Radiation affects the synthesis of lens proteins. Decreased incorporation of amino acids into proteins with decreased levels of soluble lens protein is produced (Dische et al, 1959). Nutritional Cataract In experimental animals, cataracts could be produced by feeding diet deficient of essential amino acids and certain vitamins. The essential amino acids are necessary for the elaboration of lenticular proteins and vitamins are necessary for the continuance of the metabolism. The occurrence of cataract due to lack of essential amino acids is more firmly established. Most of the experimental work has been done on rats. In this connection the most important amino acid is tryptophan. The mechanism for tryptophan deficiency cataractogenesis is unknown, but the available evidence suggests that there is a failure in the supply of nicotinic acid which is produced from tryptophan. Less dramatic results have been reported following the lack of other indispensable amino acids with the exception of arginine, phenylalanine, histidine and methionine. It would seen that the occurrence of cataract is due to the arrest of the synthesis of soluble proteins and is associated with a general arrest of growth, cutaneous lesions and vascularization of the cornea. A deficiency of vitamins, particularly those of the B2 (Riboflavin) has been claimed to result in the development of cataract. 27 Traumatic Cataract Trauma to the eye, or more specifically to the lens, can cause cataract but the mechanism is obscure. With a rupture of the capsule, different conditions arise owing to the entrance of the aqueous, the loss of essential diffusible substances and rapid proteolysis with the development of a localized or a complete opacity. Cold Cataract If the isolated lens of a young animal is frozen, it turns completely opaque and on thawing clears up from the periphery. The Taction is due to the precipitation of gamma crystallin when cooling reaches a temperature below 10°C, a reaction is reversed on warming above this temperature. The cold precipitation possibly occurs as this proteins possesses a large number of exposed hydrophobic groups. If the fraction of gamma crystallin is greater than 0.3%, other proteins increase the solubility of the total protein by hydrophobic bonding with the gamma crystallin. Therefore, young animals are more susceptible to cold cataract since at an early age the gamma crystallin constitutes the major part of the proteins of the lens. Genetic Cataract Lowe's syndrome is a recessive sex-linked trait characterized biochemically by hyperamino aciduria and abnormal ammonia metabolism. Among other symptoms it affects the eyes by causing cataract or glaucoma. Its effect on the lens appears to be mediated by reducing the availability of amino acids for synthesis of lenticular proteins.
Load more

Recommended publications
  • Genes in Eyecare Geneseyedoc 3 W.M
    Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease.
    [Show full text]
  • Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract
    Hindawi Journal of Diabetes Research Volume 2017, Article ID 3472735, 8 pages https://doi.org/10.1155/2017/3472735 Research Article Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract 1 2 1 Lixia Ji, Lixia Cheng, and Zhihong Yang 1Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China 2Department of Endocrinology, People’s Hospital of Weifang, Weifang, China Correspondence should be addressed to Lixia Ji; [email protected] Received 21 September 2017; Accepted 1 November 2017; Published 21 November 2017 Academic Editor: Hiroshi Okamoto Copyright © 2017 Lixia Ji et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Lens osmotic expansion, provoked by overactivated aldose reductase (AR), is the most essential event of sugar cataract. Chloride channel 3 (Clcn3) is a volume-sensitive channel, mainly participating in the regulation of cell fundamental volume, and P-glycoprotein (P-gp) acts as its modulator. We aim to study whether P-gp and Clcn3 are involved in lens osmotic expansion of galactosemic cataract. Methods and Results. In vitro, lens epithelial cells (LECs) were primarily cultured in gradient galactose medium (10–60 mM), more and more vacuoles appeared in LEC cytoplasm, and mRNA and protein levels of AR, P-gp, and Clcn3 were synchronously upregulated along with the increase of galactose concentration. In vivo, we focused on the early stage of rat galactosemic cataract, amount of vacuoles arose from equatorial area and scattered to the whole anterior capsule of lenses from the 3rd day to the 9th day, and mRNA and protein levels of P-gp and Clcn3 reached the peak around the 9th or 12th day.
    [Show full text]
  • Sudheendran-Dissertation
    © Copyright by Narendran Sudheendran 2013 All Rights Reserved STUDYING MOUSE EMBRYONIC DEVELOPMENT WITH OCT A Dissertation Presented to the Faculty of the Department of Biomedical Engineering University of Houston In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy in Biomedical Engineering by Narendran Sudheendran December 2013 STUDYING MOUSE EMBRYONIC DEVELOPMENT WITH OCT ___________________________ Narendran Sudheendran Approved: ________________________________ Chair of the Committee Kirill V. Larin, Associate Professor, Department of Biomedical Engineering Committee Members: ________________________________ Irina V. Larina, Assistant Professor, Department of Molecular Physiology and Biophysics, Baylor College of Medicine ________________________________ Rajesh C. Miranda, Associate Professor, Department of Neuroscience and Experimental Therapeutics, TAMHSC College of Medicine _______________________________ Howard Gifford, Associate Professor, Department of Biomedical Engineering _______________________________ Yingchun Zhang, Assistant Professor, Department of Biomedical Engineering ____________________________ _______________________________ Suresh K. Khator, Associate Dean, Metin Akay, Professor and Chairman, Cullen College of Engineering Department of Biomedical Engineering ACKNOWLEDGEMENTS I am extremely thankful to my advisor, Dr. Kirill Larin, for his guidance, support and encouragement throughout this work. I am extremely grateful to Dr. Irina Larina for her time and effort to help me during the entire course of my project. I would especially like to thank Saba, Maleeha, Dr. Shameena Bake and Chen for helping me with the experiments. I thank Esteban, Shang and Manmohan for reviewing my dissertation. I am thankful to Mohamad, Kiran, Venu, Stepan, Jiasong, Peter and the rest of the BOL team for their support and encouragement. I would like to thank Dr. Rajesh C. Miranda and Dr. Howard Gifford and Dr. Yingchun Zhang for their time to serve on my defense committee.
    [Show full text]
  • Dismetabolic Cataracts
    ndrom Sy es tic & e G n e e n G e f T o Journal of Genetic Syndromes Cavallini et al., J Genet Syndr Gene Ther 2013, 4:7 h l e a r n a r p u DOI: 10.4172/2157-7412.1000165 y o J & Gene Therapy ISSN: 2157-7412 Case Report Open Access Dismetabolic Cataracts: Clinicopathologic Overview and Surgical Management with B-MICS Technique Cavallini GM1, Forlini M1, Masini C1, Campi L1, Chiesi C1, Rejdak R2 and Forlini C3* 1Institute of Ophthalmology, University of Modena, Modena, Italy 2Department of Ophthalmology, Medical University of Lublin, Lublin, Poland 3Department of Ophthalmology, “Santa Maria Delle Croci” Hospital, Ravenna, Italy Abstract Background: Dismetabolic cataract is a loss of lens transparency due to an insult to the nuclear or lenticular fibers, caused by a metabolic disorder. The lens opacification may occur early or later in life, and may be isolated or associated to particular syndromes. We describe some of these metabolic conditions associated with cataract formation, and in particular we report our experience with a patient affected by lathosterolosis that presented bilateral cataracts. Methods: Our patient was a 7-years-old little girl diagnosed with lathosterolosis at age 2 years, through gas cromatography/mass spectrometry method for plasma sterol profile that revealed a peak corresponding to cholest- 7-en-3β-ol (lathosterol). Results: The lens samples obtained during surgical removal with B-MICS technique were sent to the Department of Pathology and routinely processed and stained with haematoxylin-eosin and PAS; then, they were examined under a light microscope. Histological examination revealed lens fragments with the presence of fibers disposed in a honeycomb way, samples characterized by the presence of homogeneous eosinophilic lens fibers, and other fragments characterized by bulgy elements referable to cortical fibers with degenerative characteristics.
    [Show full text]
  • Textbook of Ophthalmology, 5Th Edition
    Textbook of Ophthalmology Textbook of Ophthalmology 5th Edition HV Nema Former Professor and Head Department of Ophthalmology Institute of Medical Sciences Banaras Hindu University Varanasi India Nitin Nema MS Dip NB Assistant Professor Department of Ophthalmology Sri Aurobindo Institute of Medical Sciences Indore India ® JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD. New Delhi • Ahmedabad • Bengaluru • Chennai Hyderabad • Kochi • Kolkata • Lucknow • Mumbai • Nagpur Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110 002 I ndia Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672 Rel: +91-11-32558559 Fax: +91-11-23276490 +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094, e-mail: [email protected] 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001, Phones: +91-80-22285971, +91-80-22382956, 91-80-22372664 Rel: +91-80-32714073, Fax: +91-80-22281761 e-mail: [email protected] 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897 Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: [email protected] No. 41/3098, B & B1, Kuruvi Building, St.
    [Show full text]
  • In Vitro Anticataract Activity of Tamarindus Indica Linn. Againest Glucose-Induced Cataractogenisis
    Results IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA LINN. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS Dissertation submitted to The Tamil Nadu Dr. M. G. R. Medical University, Chennai in partial fulfillment of the award of degree of MASTER OF PHARMACY (PHARMACOLOGY) Submitted by SRIKANTH MERUGU Under the guidance of Mrs. M. UMA MAHESWARI, M. Pharm., (Ph.D.,) Assistant Professor, Department of Pharmacology MARCH – 2009 COLLEGE OF PHARMACY SRI RAMAKRISHNA INSTITUTE OF PARAMEDICAL SCIENCES COIMBATORE – 641 044. 1 Results IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA LINN. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS Dissertation submitted to The Tamil Nadu Dr. M. G. R. Medical University, Chennai in partial fulfillment of the award of degree of MASTER OF PHARMACY (PHARMACOLOGY) MARCH – 2009 COLLEGE OF PHARMACY SRI RAMAKRISHNA INSTITUTE OF PARAMEDICAL SCIENCES COIMBATORE – 641 044. 2 Results CERTIFICATE This is to certify that the dissertation entitled “IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA L. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS” being submitted to The Tamil Nadu Dr. M.G.R. Medical University, Chennai in partial fulfillment of the Master of Pharmacy programme in Pharmacology, carried out by Mr. SRIKANTH MERUGU in the Department of Pharmacology, College of Pharmacy, SRIPMS, Coimbatore, under my direct guidance and supervision to my fullest satisfaction. Mrs. M. UMA MAHESWARI, M.Pharm., (Ph.D.,) Assistant Professor, Dept. In-charge Department of Pharmacology, College of Pharmacy, SRIPMS, Place: Coimbatore Coimbatore –44. Date: 3 Results CERTIFICATE This is to certify that the dissertation entitled “IN VITRO ANTICATARACT ACTIVITY OF TAMARINDUS INDICA L. AGAINEST GLUCOSE-INDUCED CATARACTOGENISIS.” was carried out by Mr. SRIKANTH MERUGU, in the Department of Pharmacology, College of Pharmacy, Sri Ramakrishna Institute of Paramedical Sciences, Coimbatore, which is affiliated to The Tamil Nadu Dr.
    [Show full text]
  • Old Theories and New Ideas on Ocular Function
    Old Theories and New Ideas on Ocular Function Can the Choroid Affect ination in cadavers, to demonstrate that associated with its hyperproliferative Primate Eye Size? only the global layer of each rectus ex- property. ■ traocular muscle inserts on and rotates Earlier studies with chicks have shown the eye. The orbital layer instead inserts that choroid thickness is actively regu- on that muscle’s connective tissue pul- lated in response to retinal defocus and ley, translating it along the muscle axis. Is Glaucoma Only a may be involved in the regulation of eye This finding implies that pulleys, which Disease of the Eye? growth. In two articles in this issue, act as functional origins of the extraoc- Glaucoma is a disease of the optic nerve Troilo et al. (p. 1249) and Hung et al. (p. ular muscles, are under powerful active that also results in the degeneration of 1259) independently show that the pri- control. ■ mate choroid also undergoes changes ganglion cells within the retina. While in thickness associated with visual ex- glaucomatous changes within the retina perience and experimentally induced Is ‘Visual Acuity’ the Best and optic nerve are well-described, little changes in eye size and refraction. Measure of Visual is known about the degeneration that There is some evidence that these occurs postsynaptically within the LGN, changes, although much smaller than Function? a primary site of visual integration. This those seen in chick, might also partially Is visual acuity the most appropriate vi- study by Weber et al. (p. 1370) shows compensate for imposed retinal de- sual function to measure in determining that glaucoma has a significant effect on focus.
    [Show full text]
  • Review Article Does Phacoemulsification Speed the Progression of Diabetic Retinopathy? a Meta-Analysis
    Int J Clin Exp Med 2016;9(6):8874-8882 www.ijcem.com /ISSN:1940-5901/IJCEM0019867 Review Article Does phacoemulsification speed the progression of diabetic retinopathy? A meta-analysis Shengxia Wang1,2, Qian Xu2, Yunhong Du2, Xinyi Wu1 1Department of Ophthalmology, Qilu Hospital of Shandong University, 107 Wenhua Xi Road, Jinan 250012, Shandong, People’s Republic of China; 2Department of Ophthalmology, The Central Hospital of Tai’an, 29 Longtan Road, Taishan, Tai’an 271000, Shandong, People’s Republic of China Received November 16, 2015; Accepted April 14, 2016; Epub June 15, 2016; Published June 30, 2016 Abstract: The objective of the present study is to evaluate the influence of phacoemulsification on postoperative progression of diabetic retinopathy and incidence of diabetic macular edema in patients with diabetes and cataract. To perform a meta-analysis for this study, the computerized databases including Medline, Embase and Cochrane library were searched to identify eligible studies, in which patients with diabetes and cataract received phacoemul- sification in one eye and the non-operated contralateral eye was considered as the control group. The progression rate of diabetic retinopathy and incidence of diabetic macular edema in two study groups were extracted from the enrolled articles. Statistical analyses were performed using CMA-2 software, where dichotomous variables were ex- pressed as odds ratio (OR) and 95% confidence intervals. As a result, a total of 7 articles were eventually included in this meta-analysis. Both the progression rate of diabetic retinopathy and incidence of diabetic macular edema in the operated eye after phacoemulsification (OR=1.53, 95% CI: 1.04-2.26, P=0.03) was higher than the non-operated contralateral control (OR=1.86, 95% CI: 1.03-3.37, P=0.04).
    [Show full text]
  • Possibility of Clinical Application of Vitamin E to Cataract Prevention
    Serial Review J. Clin. Biochem. Nutr., 35, 35–45, 2004 Vitamin E Guest Editor: Etsuo Niki Possibility of Clinical Application of Vitamin E to Cataract Prevention Yoshiji Ohta* Department of Chemistry, School of Medicine, Fujita Health University, Toyoake 470–1192, Japan Received 30 October, 2003; Accepted 10 November, 2003 Summary It has been implicated that oxidative stress is involved in the development of aged-related and diabetic cataracts in humans and also in cataract development in a variety of in vivo experimental cataract models. Therefore, this article will review the possibility of the clinical application of vitamin E to cataract prevention, based on data concerning the level of vitamin E in normal and cataractous lenses of humans and experimental animals, the relationship between dietary vitamin E intake and the risk of cataracts, the effect of vita- min E supplementation on cataract development in humans, and the effect of oral or parenteral vitamin E treatment or topical vitamin E instillation on cataract development in a variety of in vivo experimental cataract models. These data reported so far may allow us to think of a possibility that vitamin E is clinically applied to cataract development. Key Words: cataract (humans and experimental animals), oxidative stress, vitamin E, cataract prevention Cataract treatment in humans is now conducted Introduction by surgical operation, i.e., cataract surgery, and then intraocular lenses are inserted into the cataract sur- Cataract is the major cause of blindness world- gery-operated eyes to recover visual acuity. However, wide. About 40% of the estimated 42 million blind an ideal treatment of cataracts is carried out without people worldwide are blind from cataract [1].
    [Show full text]
  • Radical Scavenger and Active Oxygen Eliminating Agent
    (19) TZZ__T (11) EP 1 897 549 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: A61K 31/198 (2006.01) 24.08.2011 Bulletin 2011/34 (86) International application number: (21) Application number: 06757009.3 PCT/JP2006/311269 (22) Date of filing: 06.06.2006 (87) International publication number: WO 2006/132205 (14.12.2006 Gazette 2006/50) (54) RADICAL SCAVENGER AND ACTIVE OXYGEN ELIMINATING AGENT RADIKALFÄNGER UND AKTIVEN-SAUERSTOFF-ELIMINIERENDES MITTEL PIÈGE À RADICAUX ET AGENT D’ÉLIMINATION DE L’OXYGÈNE ACTIF (84) Designated Contracting States: • SPENCER J P E ET AL: "Conjugates of AT BE BG CH CY CZ DE DK EE ES FI FR GB GR catecholamines with cysteine and GSH in HU IE IS IT LI LT LU LV MC NL PL PT RO SE SI Parkinson’s disease: Possible mechanisms of SK TR formation involving reactive oxygen species" JOURNAL OF NEUROCHEMISTRY 199811 US, (30) Priority: 07.06.2005 JP 2005166842 vol. 71, no. 5, November 1998 (1998-11), pages 2112-2122, XP002538225 ISSN: 0022-3042 (43) Date of publication of application: • AKIYAMA N ET AL: "Involvement of H2O2 and 12.03.2008 Bulletin 2008/11 O2<-> in the cytotoxicity of N-[beta]-alanyl-5-S- glutathionyl-3,4-dihyd roxyphenylalanine (5-S- (73) Proprietor: InBiotex Inc. GAD), a novel insect-derived anti-tumor Bunkyo-ku, Tokyo 1130033 (JP) compound" CANCER SCIENCE 20030401 JP, vol. 94,no.4,1April2003(2003-04-01),pages400-404, (72) Inventors: XP002538226 ISSN: 1347-9032 • NATORI, Shunji • JAE YOON LEEM ET AL: "Purification and Ibaraki characterization of N-[beta]-alanyl-5-S- 3001622 (JP) glutathionyl 3,4- dihydroxyphenylalanine, a • OOTSU, Kunimiki novel antibacterial substance of Sarcophaga 1950071 (JP) peregrina (flesh fly)" JOURNAL OF BIOLOGICAL • OKUYAMA, Hajime CHEMISTRY 1996 US, vol.
    [Show full text]
  • Postoperative Intraocular Pressure After Cataract Surgery: Influence of Surgical Technique and Antiglaucoma Medication
    Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Doctoral thesis at the Medical University of Vienna for obtaining the academic degree Doctor of Medicine (Dr. med. univ.) Submitted by Ali Asadi Supervisor Univ. Prof. Dr. med. Georg Rainer Department of Ophthalmology, Medical University of Vienna Vienna, 05.2011 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Danksagung Ich bin meinem Betreuer Herrn Univ. Prof. Dr. Georg Rainer zu großem Dank verpflichtet. Er hat mich stetig betreut, unterstützt, professionell angeleitet und mir einen breiten Einblick in die Behandlung dieses Themas und generell in das wissenschaftliche Arbeiten gewährt. 2 Postoperative intraocular pressure after cataract surgery: Influence of surgical technique and antiglaucoma medication Zusammenfassung: Die Standardoperationstechnik in der Kataraktchirurgie ist derzeit die Phakoemulsifikation mit Implantation einer faltbaren Intraokularlinse unter Einsatz von viskochirurgischen Substanzen. Die häufigste Spätkomplikation nach der Kataraktoperation ist der Nachstar, eine Trübung der hinteren Linsenkapsel. Daher werden chirurgische Methoden untersucht, die den Nachstar verhindern können. Es konnte gezeigt werden, dass die Operationstechnik mit Präparation einer kreisrunden Öffnung in der hinteren Linsenkapsel (hintere Kapsulorhexis) den Nachstar wirksam verhindern kann. Diese Operationstechnik könnte jedoch zu einem höheren postoperativen
    [Show full text]
  • Nonenzymatic Glycosylation, Sulfhydryl Oxidation, and Aggregation of Lens Proteins in Experimental Sugar Cataracts*
    NONENZYMATIC GLYCOSYLATION, SULFHYDRYL OXIDATION, AND AGGREGATION OF LENS PROTEINS IN EXPERIMENTAL SUGAR CATARACTS* BY V. M. MONNIER, V. J. STEVENS,~ AND A. CERAMI From the Laboratory of Medical Biochemistry, The Rockefeller University, New York 10021 In studies of human cataracts, Dische and Zil (I) first noted that the proteins of the human cataractous lens were associated with a marked increase in sulflaydryl oxidation to form disulfide bonds. The correlation of disulfide bonds and cataract formation has been combined subsequently by a number of other workers studying animal and human cataracts (2-6). These disulfide bonds can act as intermolecular crosslinks and have been proposed to be partly responsible for the polymerization of the lens proteins in the formation of high molecular weight aggregates. Protein aggregates > 150 × 106 dahons have been detected in aged normal lenses as well as in human cataracts (7, 8) and recently a disulfide-linked high molecular weight protein associated with the fiber cell membrane has been isolated from human cataracts and characterized (9). One of the physical characteristics of protein aggregates of this size is their ability to scatter light. Based on theoretical consideration, Benedek (10) has hypothesized that the formation of protein aggregates of tool wt > 50 × 106 dahons could scatter light sufficiently to account for cataract formation in the lens. This is substantiated by the work of Spector and colleagues (11) who found that light backscattering of the lens parallels the increase in high molecular weight protein in the aging lens. In contrast to studies of human senile cataractogenesis, little is known of the physical state of the lens proteins of the sugar cataracts formed in diabetes and galactosemia.
    [Show full text]