Nitric oxide participates in cataract development in selenite-treated rats

Ito, Yoshimasa; Nabekura, Tomohiro; Takeda, Maki; Nakao, Motoki; Terao, Motome; Hori, Ryohei; Tomohiro, Masayuki

doi:10.1076/ceyr.22.3.215.5516

Cited by 50 publications

(38 citation statements)

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“…17) We previously reported that the increase in Ca 2ϩ concentration in lenses resulted in cataract development in cataract model rats, and the induction of iNOS protein occurred prior to the elevation of Ca 2ϩ content in the lenses. [18][19][20] In addition, the administration of disulfiram, a dimer of DDC, and AG can prevent lens opacification in the Shumiya cataract rat (SCR), UPL rat, and selenite-induced cataract rat. [18][19][20] Nitric oxide (NO) is synthesized from the guanidino-nitrogen of L-arginine and molecular oxygen by NOS.…”

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confidence: 99%

“…[18][19][20] In addition, the administration of disulfiram, a dimer of DDC, and AG can prevent lens opacification in the Shumiya cataract rat (SCR), UPL rat, and selenite-induced cataract rat. [18][19][20] Nitric oxide (NO) is synthesized from the guanidino-nitrogen of L-arginine and molecular oxygen by NOS. iNOS, one of the three isoforms of NOS, 21) is usually not present under normal conditions, is Ca 2ϩ independent, and induced by cytokines, such as interferon-gamma (IFN-g) and tumor necrosis factor a (TNF-a).…”

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Inhibitors of Inducible Nitric Oxide Synthase Prevent Damage to Human Lens Epithelial Cells Induced by Interferon-Gamma and Lipopolysaccharide

Nagai

Liu

Fukuhata

et al. 2006

Biological & Pharmaceutical Bulletin

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Inhibitors of Inducible Nitric Oxide Synthase Prevent Damage to Human Lens Epithelial Cells Induced by Interferon-Gamma and Lipopolysaccharide

Nagai

Liu

Fukuhata

et al. 2006

Biological & Pharmaceutical Bulletin

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“…Selenite causes increasing lipid peroxidation and oxidation of sulfhydryl groups and damage of membranes of lens fibres. This mechanism resembles age-related cataract [23]. These processes lead to protein aggregation and result in a decrease the water soluble proteins followed by opacification of the lens [24,25].…”

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confidence: 99%

The Anti-Cataract Effect of Coenzyme Q10 in Rabbits

Hussein

Mahmood

2017

Int J Pharm Pharm Sci

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Objective: cataract is the opacity of the lens which progressively impairs the light transmission to the retina and finally prevents the vision, these opacity result from the oxidative process in the eye. The study aimed to prevent opacity of the lens by using Coenzyme Q10 as eye drops.Methods: Sodium selenite 0.01w/v injected intravitreal to the rabbit's eye to induce the disease, a group of rabbits were receive Coenzyme Q10 eye drop, and another group received distilled water, pre and post induction, cataract maturity was measured to evaluate the opacity deterioration.Results: the group of rabbits that received distilled water after induction of cataract, the opacity occurred within 48-72 h and the mean score of opacity reached to (4±0.00), while Coenzyme Q10 treated group the degree of opacity was (1.5±0.02), and there was a highly significant difference (p<0.01). Conclusion:Coenzyme q10 has an antioxidant activity when use as eye drops and this effect enable Coenzyme Q10 to prevent the opacity which is the major cause of cataract due to oxidative stress.

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“…Magnesium deficiency has been shown to cause increased oxidative stress and trigger cataractogenesis by increasing inducible NO synthase (iNOS) expression and NO release. Pretreatment of rats with NO synthase inhibitors has been shown to prevent onset of selenite-induced cataract and reduce lens calcium content [95]. Culture of human lens epithelial cells in magnesium deficient medium shows 6 fold increase in expression of İNOS as compared to those cultured in medium with normal magnesium concentration.…”

Section: Magnesium: Have a Role In Cataractogenesis?mentioning

confidence: 99%

Magnesium: Effect on ocular health as a calcium channel antagonist

Korkmaz

Ekici²,

Tufan³

et al. 2013

J Clin Exp Invest

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ÖZETMagnezyum hücre zar fonksiyonlarını, düz kas kontraksiyonlarını ve enzimatik reaksiyonları etkileyerek pek çok metabolik sürece katılan fizyolojik bir kalsiyum kanal blokörüdür. Magnezyumun Endothelin-1 (ET-1) ve Nitrik Oksit (NO) yolakları vasıtasıyla endotel fonksiyonları-nı modifiye ederek dokulara kan akımında artışa neden olduğu gösterilmiştir. Magnezyum aynı zamanda N-metil-D-aspartat (NMDA) reseptör ilişkili kalsiyum içe akımı-nı bloke ederek ve glutamat serbestleşmesini önleyerek nöroprotektif rol oynamakta ve hücreleri oksidatif stres ve apoptoza karşı korumaktadır. Hem kan akımında artışa neden olması hem de nöroprotektif etkileri magnezyumu glokom çalışmaları için iyi bir hedef molekül yapmaktadır. Magnezyumun retinada oksidatif stresi ve apoptozu azalttığı ve ganglion koruyucu etkileri olduğu gösterilmiştir. Bir takım çalışmalarda aynı zamanda magnezyumun diabetik hastalarda insulin resistansını azalttığı, glisemik kontrolü kolaylaştırdığı ve retinopatiyi önlediği gösterilmiştir. Magnezyumun lensteki iyon dengesinin sağlanmasında kritik önemi belirlenmiştir. Magnezyum eksikliğinin lentiküler oksidatif stresi arttırdığı ve iyon dengesini bozarak katarakt oluşumuna neden olduğu gösterilmiştir.Anahtar kelimeler: Magnezyum, kalsiyum kanal blokajı, glokom, nöroproteksiyon, diabetik retinopati, katarakt ABSTRACTMagnesium is the physiologic calcium channel blocker, involving in many different metabolic processes by maintaining cell membrane function, modulating smooth muscle contraction and influencing enzymatic activities. Magnesium has been shown to increase blood flow to tissues by modifying endothelial function via endothelin-1 (ET-1) and nitric Oxide (NO) pathways. Magnesium also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor related calcium influx and by inhibiting the release of glutamate, hence protects the cell against oxidative stress and apoptosis. Both increase in blood flow and its neuroprotective effect make magnesium a good candidate for glaucoma studies. Magnesium has been shown to decrease oxidative stress and apoptosis in retinal tissue and to have retinal ganglion cell sparing effect. A series of studies has been conducted about magnesium could decrease insulin resistance in diabetic patients, ease glycemia control and prevent diabetic retinopathy. Magnesium is found to be critically important in maintaining normal ionic homeostasis of lens. Magnesium deficiency has been shown to cause increased lenticular oxidative stress and ionic imbalance in the lens so trigger cataractogenesis. J Clin Exp Invest 2013; 4 (2): 244-251

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Nitric oxide participates in cataract development in selenite-treated rats

Abstract: The present study demonstrated that NOS inhibitors prevented the development of cataracts in selenite-treated rats. The results also suggest that nitric oxide had an important role in the development of selenite-induced cataracts.

Cited by 50 publications

References 17 publications

Inhibitors of Inducible Nitric Oxide Synthase Prevent Damage to Human Lens Epithelial Cells Induced by Interferon-Gamma and Lipopolysaccharide

Inhibitors of Inducible Nitric Oxide Synthase Prevent Damage to Human Lens Epithelial Cells Induced by Interferon-Gamma and Lipopolysaccharide

The Anti-Cataract Effect of Coenzyme Q10 in Rabbits

Magnesium: Effect on ocular health as a calcium channel antagonist

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