Changes in Blood Antioxidants and Several Lipid Peroxidation Products in Women with Age-Related Macular Degeneration

Nowak, Mariusz; Świętochowska, Elżbieta; Wielkoszyński, Tomasz; Marek, Bogdan; Karpe, Jacek; Gorski, Joel R.; Głogowska-Szeląg, Joanna; Kos–Kudła, Beata; Ostrowska, Zofia

doi:10.1177/112067210301300307

Cited by 46 publications

(30 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In one of the study reports, while estimating the enzymatic and nonenzymatic components of the antioxidant system it was shown that the average concentrations of vitamin A and C were low and vitamin E and GSH were significantly higher in patients with ARMD than in the control group, with the activity of almost all the antioxidant enzymes being high, showing that there is an adaptive increase in the antioxidant barrier of mostly the enzymatic components. 27 The multicentre, double-blind cross-sectional study reported by Everklioglu et al has shown that late ARMD patients had significantly lower antioxidant enzyme levels and higher MDA levels when compared with early ARMD patients, which may reflect the levels of the various antioxidants including GSH. 16 Therefore, grouping of the patients based on the clinical picture seems to be crucial before arriving at conclusions.…”

Section: Discussionmentioning

confidence: 97%

Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration

Coral

Raman

Rathi

et al. 2005

Eye

View full text Add to dashboard Cite

Purpose Exudative age-related macular degeneration (ARMD) is one of the debilitating ocular complications, which results in permanent blindness. Elevated homocysteine (Hcys) levels have been associated in the development of several vascular diseases. Vascular and oxidative stress theories have been implicated for the development of choroidal neovascularization in exudative ARMD. The aim of the present study was to investigate the possible role of plasma Hcys and thiol content (tSH) as a risk factor for the development of exudative ARMD. Method A total of 16 patients with exudative ARMD and 20 age-matched controls were recruited for the study. Plasma Hcys levels were analysed using Reverse Phase High Performance Liquid Chromatography. Plasma glutathione (GSH) content was determined using o-phthalaldehyde (OPA) derivatization and subsequent detection by fluorimeter. Plasma tSH levels were determined by using thiol-specific reagent dithionitrobenzoic acid (DTNB) spectrophotometrically. Results Plasma Hcys levels in exudative ARMD were elevated three-fold (1875.0 lM) when compared to healthy controls (6.771.8 lM). There was a two-fold decrease in the GSH and tSH in exudative ARMD when compared with controls. Negative correlation was observed between diminished tSH and Hcys levels (r ¼ À0.4837, P ¼ 0.05). Similarly plasma Hcys levels negatively correlated with GSH content (r ¼ À0.6620, Po0.05). Conclusion Results from our present study revealed that there is an elevated Hcys level and diminished thiol pool content in exudative ARMD that are significant.

show abstract

Section: Discussionmentioning

confidence: 97%

Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration

Coral

Raman

Rathi

et al. 2005

Eye

View full text Add to dashboard Cite

show abstract

“…It has been suggested that lipid peroxidation may play an important role in the degeneration of photoreceptors and RPE cells (10,41). Therefore, we examined whether retinaldehyde-induced photooxidative toxicity caused lipid peroxidation in ARPE-19 cells and whether the magnitude of lipid peroxidation correlated with the cytotoxicity.…”

Section: Phototoxicity Of Retinoidsmentioning

confidence: 96%

Induction of phase 2 genes by sulforaphane protects retinal pigment epithelial cells against photooxidative damage

Gao

Talalay

2004

Proc. Natl. Acad. Sci. U.S.A.

207

174

View full text Add to dashboard Cite

The retinal pigment epithelial cell (RPE cell) layer protects the photoreceptors of the retina against oxidative stress. The decline of this capacity is believed to be a major factor in the impairment of vision in age-related macular degeneration. Exposure of human adult RPE cells to UV light at predominantly 320 -400 nm (UVA light) in the presence of all-trans-retinaldehyde results in photooxidative cytotoxicity. Significant protection of RPE cells was obtained by prior treatment with phase 2 gene inducers, such as the isothiocyanate sulforaphane or a bis-2-hydroxybenzylideneacetone Michael reaction acceptor. The degree of protection was correlated with the potencies of these inducers in elevating cytoprotective glutathione levels and activities of NAD(P)H:quinone oxidoreductase. In embryonic fibroblasts derived from mice in which the genes for the transcription factor Nrf2, the repressor Keap1, or both Nrf2 and Keap1 were disrupted, the magnitude of resistance to photooxidative damage paralleled the basal levels of glutathione and NAD(P)H:quinone oxidoreductase in each cell type. Demonstration of protection of RPE cells against photooxidative damage by induction of phase 2 proteins may shed light on the role of oxidative injury in ocular disease. Moreover, the finding that dietary inducers provide indirect antioxidant protection suggests novel strategies for preventing chronic degenerative diseases, such as age-related macular degeneration. Because oxidative damage is widely believed to contribute to the etiology and progression of many age-related chronic degenerative diseases, the development of methods for antioxidant protection is a priority and may be broadly relevant to disease prevention (1). Here, we describe a strategy for protecting retinal pigment epithelial cells (RPE cells) against photooxidative damage by coordinate elevation (induction) of the activities of a family of phase 2 genes that protect cells against injury by oxidants and electrophiles (2-5). This study complements and extends our recent demonstration that sulforaphane, a potent phase 2 gene inducer, protects human adult RPE cells against the cytotoxicity of the following oxidants: tert-butyl hydroperoxide, menadione, 4-hydroxynonenal, and peroxynitrite (6). The magnitude of this protection is correlated quantitatively with the elevation of phase 2 genes and glutathione (GSH) levels (6). Jones, Sternberg, and colleagues (7,8) have also demonstrated protection of RPE cells against oxidative damage by elevation of GSH levels and induction of the phase 2 response.Oxidative damage has been implicated in the etiology of age-related macular degeneration (AMD), which is the leading cause of blindness among the elderly. AMD entails progressive degeneration of both macular photoreceptors and associated RPE cells. This photoreceptor loss is widely believed to be, in part, secondary to degenerative changes in the RPE layer. Two significant risk indicators for AMD are the formation of drusen and the accumulation of lipofuscin within RPE cells. Dru...

show abstract

“…Levels of lipidperoxidation products are also increased with aging (44,83,87,97,108,113,119,123). In addition, aging-related oxidative modification of different proteins causes changes in protein structure, enzyme activities, transcriptional activities, and signal-transduction pathways (32,70,103,111,112,124), leading to age-related diseases.…”

Section: Liu and Xumentioning

confidence: 99%

p53, Oxidative Stress, and Aging

Liu

Xu²

2011

Antioxidants & Redox Signaling

272

198

View full text Add to dashboard Cite

Mammalian aging is associated with elevated levels of oxidative damage of DNA, proteins, and lipids as a result of unbalanced prooxidant and antioxidant activities. Accumulating evidence indicates that oxidative stress is a major physiological inducer of aging. p53, the guardian of the genome that is important for cellular responses to oxidative stresses, might be a key coordinator of oxidative stress and aging. In response to low levels of oxidative stresses, p53 exhibits antioxidant activities to eliminate oxidative stress and ensure cell survival; in response to high levels of oxidative stresses, p53 exhibits prooxidative activities that further increase the levels of stresses, leading to cell death. p53 accomplishes these context-dependent roles by regulating the expression of a panel of genes involved in cellular responses to oxidative stresses and by modulating other pathways important for oxidative stress responses. The mechanism that switches p53 function from antioxidant to prooxidant remains unclear, but could account for the findings that increased p53 activities have been linked to both accelerated aging and increased life span in mice. Therefore, a balance of p53 antioxidant and prooxidant activities in response to oxidative stresses could be important for longevity by suppressing the accumulation of oxidative stresses and DNA damage. Antioxid. Redox Signal. 15, 1669-1678.p53 Is a Critical Tumor Suppressor

show abstract

Changes in Blood Antioxidants and Several Lipid Peroxidation Products in Women with Age-Related Macular Degeneration

Cited by 46 publications

References 29 publications

Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration

Plasma homocysteine and total thiol content in patients with exudative age-related macular degeneration

Induction of phase 2 genes by sulforaphane protects retinal pigment epithelial cells against photooxidative damage

p53, Oxidative Stress, and Aging

Contact Info

Product

Resources

About