Corneal Changes in Magnesium-Deficient Rats

Gong, Huaqing; Takami, Yumiko; Kitaoka, Takashi; Amemiya, Tsugio

doi:10.1097/00003226-200307000-00011

Cited by 8 publications

(7 citation statements)

References 18 publications

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“…A series of studies on Zn [14], Mg [16] and Mn [15] deficiencies showed some corneal changes similar to those seen in riboflavin deficiency. The deficiency of these essential trace elements may lead to cell degeneration as well as lowered activity of the superoxide dismutases (SOD) Zn W Cu-SOD and Mn-SOD [20].…”

Section: Discussionmentioning

confidence: 93%

“…Abnormal secretion in riboflavin deficiency may be one of these disturbances. On the other hand, the changes in the cornea are specific for riboflavin deficiency and not seen in other micronutrient deficiencies such as those of Zn [14], Mn [15], Mg [16], Cr, and vitamins A [17] and C. The reduction of microvilli and microplicae in the corneal surface is common in those micronutrient deficiencies, but only riboflavin deficiency induces degenerative changes of the wing cells, onion-shaped dense deposits in the subepithelial area, and degenerative stroma cells. The significance of dense deposits in the subepithelial stroma is unclear, but we assume that degeneratedwing cells are released to the subepithelial stroma through basal cells and dense deposits represent cellular debris, because epithelial cells generally release waste products from the basal portion like the dense deposits in Bruch's membrane [18,19].…”

Section: Discussionmentioning

confidence: 99%

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Riboflavin Deficiency Induces Ocular Surface Damage

Takami

Gong

Amemiya³

2004

Ophthalmic Res

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Purpose: To examine the conjunctiva and cornea of riboflavin-deficient rats with scanning (SEM) and transmission (TEM) electron microscopes. Materials and Methods: Three-week-old Wistar Kyoto rats were fed a riboflavin-deficient diet (0.05 mg riboflavin/100 g) for 3 months. As a recovery experiment, rats which had been on a riboflavin-deficient diet for 3 months were given water with 1 mg riboflavin/300 ml for 2 months. The conjunctiva and the cornea were examined with SEM and TEM. Results: The serum riboflavin level was significantly lower in the riboflavin-deficient group than in the controls. In rats on a riboflavin-deficient diet for 3 months, SEM showed decreased microvilli and microplicae in the superficial epithelium of the conjunctiva and a decrease in the number of goblet cells. The cornea showed many dark cells and a marked decrease of microvilli and microplicae. In the riboflavin-deficient rats, TEM of the conjunctiva showed a decrease of microvilli and microplicae in the most superficial epithelial cells, a decrease in the layers of the epithelium and a marked decrease in the number of goblet cells, while the cornea had decreased microvilli and microplicae in the superficial epithelium, dark wing cells, loss of the basement membrane and hemidesmosomes of basal cells, cell debris and degenerative stroma cells and deposits of dense bodies in the subepithelial layer of the stroma. In rats recovered from riboflavin deficiency, the conjunctiva and cornea showed no abnormalities. Discussion: Riboflavin plays a role in the development and maintenance of the surface structures of epithelial cells. Riboflavin may also be necessary for the development and maintenance of goblet cells. Conclusion: Riboflavin is essential for maintaining the structure and function of the ocular surface.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Riboflavin Deficiency Induces Ocular Surface Damage

Takami

Gong

Amemiya³

2004

Ophthalmic Res

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“…11,12 Trace elements deficiency, undernourishment, and exposure to drugs of abuse or alcohol induced ultrastructural changes in the ON, cornea, and retina. 25,26,29,[31][32][33][34][35][42][43][44][45][46][47][48][49][50][51][52][53] Figure 2 Mean density (a) and total number (b) of myelinated and unmyelinated fibres of the optic nerve in the control, anaemic, and recovered rats at postnatal day 32. Values are means ± SE for n ¼ 6; *Po0.05.…”

Section: Discussionmentioning

confidence: 99%

Effectiveness of iron repletion in the diet for the optic nerve development of anaemic rats

Demaman

Melo

Homem

et al. 2009

Eye

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Purpose To compare the process of myelination in the developing optic nerve (ON) of anaemic rats with the subsequent recovery after being fed an iron-recovery diet. Methods In this study, the morphometrical parameters in the ON were assessed by electron microscopy in Wistar rats that were on an iron-deficient diet for 32 days or for 21 days followed by 10 days on an iron-recovery diet. Qualitative and quantitative analyses were performed using representative electron ultramicrographs. Data were analysed by one-way analysis of variance (ANOVA). When differences were detected, comparisons were made using Tukey's post hoc test (Po0.05 was considered to be significant). Results Qualitative analysis of the ONs in anaemic and recovered animals showed a higher rate of deformed axons and increased lamellar separation in the myelin sheath when compared with the respective control group. The ON of the anaemic group showed a reduced mean density of myelinated fibres when compared with the control group. The fibre area ratio, axon area ratio, and myelin area ratio of large axons/small axons in the ONs of the control group showed the highest values for the myelin areas, axon areas, and total fibre areas. The control group showed a significantly higher myelin sheath thickness when compared with the anaemic and recovered groups. Conclusions Our data indicate that iron is necessary for maintenance of the ON cell structure, and that morphological damage from iron deficiency is not easily reverted by iron repletion.

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“…Magnesium also may be necessary for maintenance of corneal surface health which is important for protection from infections and dryness. Cornea has showed some structural changes if magnesium is missing in the developmental cycle, including decreased microvilli in the epithelial cells, nuclear changes like apoptosis in the epithelial and endothelial cells through abnormal ATP activity and abnormal ion transport [37].…”

Section: Necessity In Terms Of Eye Tissue Developmentmentioning

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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Corneal Changes in Magnesium-Deficient Rats

Cited by 8 publications

References 18 publications

Riboflavin Deficiency Induces Ocular Surface Damage

Riboflavin Deficiency Induces Ocular Surface Damage

Effectiveness of iron repletion in the diet for the optic nerve development of anaemic rats

Magnesium: Effect on ocular health as a calcium channel antagonist

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