Studies of the Mechanism of the Action of the Sodium Iodate on the Rabbit Retina

Berardinis, Ettore De; Vecchione, L; Tieri, O

doi:10.1111/j.1755-3768.1964.tb00922.x

Cited by 6 publications

(3 citation statements)

References 4 publications

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“…There have been numerous histological studies on the in vivo effect of NaIO 3 in different animal models. 26 , 36–39 Damage to the retina after NaIO 3 administration has been shown to be dose-, route-, and time-dependent. Morphological examination of the retina after 100 mg/kg NaIO 3 administration has indicated RPE depigmentation, swelling, and vacuolization, suggesting RPE necrosis in this model.…”

Section: Discussionmentioning

confidence: 99%

Retinal pigment epithelial cell necroptosis in response to sodium iodate

Hanus

Anderson

Sarraf

et al. 2016

Cell Death Discovery

114

115

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Age-related macular degeneration (AMD) is a degenerative disease of the retina and the leading cause of blindness in the elderly in developed countries. The late stage of dry AMD, or geographic atrophy (GA), is characterized by extensive retinal pigment epithelium (RPE) degeneration. The underlying molecular mechanism for RPE cell death in GA remains unclear. Our previous study has established that RPE cells die predominantly from necroptosis in response to oxidative stress in vitro. Here, we extend our study and aim to characterize the nature of RPE cell death in response to sodium iodate (NaIO3) in vitro and in a NaIO3-induced retina degeneration mouse model. We found that NaIO3 induces RPE necroptosis in vitro by using a combination of molecular hallmarks. By using TUNEL assays, active caspase-3 and HMGB1 immunostaining, we confirmed that photoreceptor cells die mainly from apoptosis and RPE cells die mainly from necroptosis in response to NaIO3 in vivo. RPE necroptosis in this model is also supported by use of the RIPK1 inhibitor, Necrostatin-1. Furthermore, using novel RIPK3-GFP transgenic mouse lines, we detected RIPK3 aggregation, a hallmark of necroptosis, in the RPE cells in vivo after NaIO3 injection. Our findings suggest the necessity of re-evaluating RPE cell death mechanism in AMD models and have the potential to influence therapeutic development for dry AMD, especially GA.

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Section: Discussionmentioning

confidence: 99%

Retinal pigment epithelial cell necroptosis in response to sodium iodate

Hanus

Anderson

Sarraf

et al. 2016

Cell Death Discovery

114

115

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“…Moreover, the increased expressions of inflammation-related proteins (complement factor C3 and calcium-independent phospholipase A2)252627, pro-angiogenic factor (IL-8)14, chemoattractant (stromal cell-derived factor-1)25, oxidative stress-related gene (heme oxygenase)26 as well as apoptotic marker (caspase-3)28 have been reported. Apart from induction of RPE cell death, sodium iodate would also cause mitochondrial dysfunction and impairment of glycolysis1629. In addition, disruption of blood-retina barrier has been indicated in sodium iodate-treated mice3031.…”

Section: Discussionmentioning

confidence: 99%

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Zhang

Brelén

et al. 2016

Sci Rep

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Age-related macular degeneration (AMD), characterized by progressive degeneration of retinal pigment epithelium (RPE), is the major cause of irreversible blindness and visual impairment in elderly population. We previously established a RPE degeneration model using an acute high dose sodium iodate to induce oxidative stress. Here we report findings on a prolonged treatment of low doses of sodium iodate on human RPE cells (ARPE-19). RPE cells were treated continuously with low doses (2–10 mM) of sodium iodate for 5 days. Low doses (2–5 mM) of sodium iodate did not reduce RPE cell viability, which is contrasting to cell apoptosis in 10 mM treatment. These low doses are sufficient to retard RPE cell migration and reduced expression of cell junction protein ZO-1. Phagocytotic activity of RPE cells was attenuated by sodium iodate dose-dependently. Sodium iodate also increased expression of FGF-2, but suppressed expression of IL-8, PDGF, TIMP-2 and VEGF. Furthermore, HTRA1 and epithelial-to-mesenchymal transition marker proteins were downregulated, whereas PERK and LC3B-II proteins were upregulated after sodium iodate treatment. These results suggested that prolonged exposure to non-lethal doses of oxidative stress induces RPE cell dysfunctions that resemble conditions in AMD. This model can be used for future drug/treatment investigation on AMD.

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“…Many investigations have indicated that iodate acts directly on the retina. The primary injury is specifically to the retinal pigment epithelium and later secondary changes include degeneration of rods and cones with pigment migration and clumping (Sorsby 1941;Noell 1953;DeBerardinis et al 1964;Nilsson et al 1977).…”

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confidence: 99%

Potassium iodate retinopathy

Singalavanija

Dongosintr

Dulayajinda

1994

Acta Ophthalmologica

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A case of potassium iodate toxicity in a 22-year-old man was reported. After taking a solution of highly concentrated potassium iodate, the patient developed nausea, vomiting, diarrhea and blurred vision. The visual acuity was hand motion in both eyes. The funduscopic examination showed retinal edema with subsequent pigmentary change at the macula and retinal pigment clumping resembling retinitis pigmentosa. The fundus fluorescein angiography and electrophysiologic studies showed degenerative changes of the retinal pigment epithelium and photoreceptor cells.

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Studies of the Mechanism of the Action of the Sodium Iodate on the Rabbit Retina

Cited by 6 publications

References 4 publications

Retinal pigment epithelial cell necroptosis in response to sodium iodate

Retinal pigment epithelial cell necroptosis in response to sodium iodate

Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction

Potassium iodate retinopathy

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