Abstract
The aim of this study was to assess the oxidative stress status in eyes affected by synchysis scintillans and to compare it to vitreoretinal disorders without synchysis scintillans. Human aqueous and vitreous humors were obtained during vitrectomy from thirty-seven otherwise healthy patients that were randomly chosen among patients that had to undergo a 25-gauge pars plana vitrectomy from the central vitreous cavity, for either synchysis scintillans (n = 16) or vitreoretinal disorders without synchysis scintillans (n = 21), such as idiopathic epimacular membrane (n = 12), macular hole (n = 5), or rhegmatogenous retinal detachment (n = 4). The redox parameters thiobarbituric acid reactive substances (TBARS), a measurement of lipid peroxidation, nitrite concentration, an estimate of nitric oxide (NO) production, 4-hydroxynonenal (4-HNE)-protein conjugates, a structural protein modification by lipid peroxidation product 4-HNE, and the antioxidative activities of Cu,Zn-superoxide dismutase (SOD), and catalase were measured in aqueous and vitreous humors and compared between synchysis scintillans affected and not-affected patients. TBARS and nitrite levels of the vitreous humor were significantly higher in patients with synchysis scintillans as compared to patients affected by vitreoretinal disorders without synchysis scintillans. Synchysis scintillans patients had significantly lower activities of SOD and catalase both in aqueous and vitreous humors than patients with vitreoretinal disorders without synchysis. The consequently higher lipoperoxide-dependent 4-HNE production in synchysis scintillans was detectable in aqueous and vitreous humors as a significant increased accumulation of 4-HNE-protein conjugates vs nonsynchysis vitreoretinal disorders. Additionally, hyaluronic acid (HA) was significantly decreased in the vitreous body of synchysis scintillans patients. The data consistently show that synchisis scintillans is accompanied by a redox imbalance with increased oxidative modifications of 4-HNE proteins and loss of HA, both of likely importance for remote damages of the retina. It remains to be proven whether a therapeutic strategy which targets oxidative stress may be effective in the treatment of synchysis patients.
Highlights
Normal aging eye is accompanied by a number of physiological changes in the vitreous gel, that is, a compact, homogeneous, and clear body at birth and that can undergo progressive degeneration characterized by vitreous liquefaction and weakening of the vitreoretinal adhesion between the posterior vitreous hyaloid and the inner limiting membrane. is degeneration, corresponding with a simultaneous decrease in gel volume, a lateral aggregation of the collagen fibrils, and a gradual destruction of the collagen-hyaluronate network, may result in posterior vitreous detachment (PVD) [1, 2]. us, PVD could increase the risks of major vitreous retinal diseases such as macular holes, epimacular membranes, vitreoretinal traction syndrome, and retinal detachment [3]
Irty-seven otherwise healthy patients were randomly chosen among patients that had to undergo a 25-gauge pars plana vitrectomy from the central vitreous cavity, for idiopathic epimacular membrane (IEM) (n = 12), macular hole (MH) (n = 5), rhegmatogenous retinal detachment (RRD) (n = 4), and synchysis scintillans (SS) (n = 16). e mean age of the patients affected by vitreoretinal disorders and synchysis scintillans was 74.0 ± 2.8 and 75.9 ± 2.1 years, respectively
Vitreous thiobarbituric acid reactive substances (TBARS) levels are significantly higher by approximately 30% in patients affected by synchysis scintillans compared to patients who underwent pars plana vitrectomy for several vitreoretinal disorders without synchysis such as idiopathic epimacular membrane (IEM), macular hole (MH), or rhegmatogenous retinal detachment (RRD) (Figure 1), indicating an increased lipid peroxidation
Summary
Normal aging eye is accompanied by a number of physiological changes in the vitreous gel, that is, a compact, homogeneous, and clear body at birth and that can undergo progressive degeneration characterized by vitreous liquefaction (synchysis) and weakening of the vitreoretinal adhesion between the posterior vitreous hyaloid and the inner limiting membrane. is degeneration, corresponding with a simultaneous decrease in gel volume, a lateral aggregation of the collagen fibrils (syneresis), and a gradual destruction of the collagen-hyaluronate network, may result in posterior vitreous detachment (PVD) [1, 2]. us, PVD could increase the risks of major vitreous retinal diseases such as macular holes, epimacular membranes, vitreoretinal traction syndrome, and retinal detachment [3].Next to vitreous retinal diseases, synchysis scintillans is a rare bilateral condition characterized by the presence of tinyJournal of Ophthalmology yellowish-white floating crystals of cholesterol in the vitreous. Normal aging eye is accompanied by a number of physiological changes in the vitreous gel, that is, a compact, homogeneous, and clear body at birth and that can undergo progressive degeneration characterized by vitreous liquefaction (synchysis) and weakening of the vitreoretinal adhesion between the posterior vitreous hyaloid and the inner limiting membrane. The senile synchysis scintillans, resulting in liquefied vitreous humor and the accumulation of cholesterol crystals within the vitreous, seems to be involved in the onset of PVD due to the possible vitreous instability, even if only a dated study was reported and performed in eyes of autopsied subjects [3]. In many vitreoretinal disorders, such as proliferative diabetic retinopathy (PDR), retinitis pigmentosa, age-related macular degeneration, and rhegmatogenous retinal detachment (RRD), OS has been implicated as a factor inducing the development of retinal cellular damage [5]
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