ArticleOxidative medicine and cellular longevity2017
Spermidine Oxidation-Mediated Degeneration of Retinal Pigment Epithelium in Rats.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Early proteomic and metabolic signatures of liver and eye in OAT-deficient mice.Experimental eye research · 2026Article
- Molecular and cellular mechanisms underlying gyrate atrophy: Why is the retina primarily affected?Acta ophthalmologica · 2025Review
- Age-related decline in retinal function in marmosets.Scientific reports · 2025Article
- Sub2Full: split spectrum to boost optical coherence tomography despeckling without clean data.Optics letters · 2024Article
- Research Progress and Potential Applications of Spermidine in Ocular Diseases.Pharmaceutics · 2022Review
- Oxidative Stress and 4-hydroxy-2-nonenal (4-HNE): Implications in the Pathogenesis and Treatment of Aging-related Diseases.Journal of immunology research · 2022Review
- Review
- Inborn errors of enzymes in glutamate metabolism.Journal of inherited metabolic disease · 2020Review
- Targeting Neurovascular Interaction in Retinal Disorders.International journal of molecular sciences · 2020Review
- Spermine oxidase: A promising therapeutic target for neurodegeneration in diabetic retinopathy.Pharmacological research · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal pigment epithelium (RPE) degeneration is a crucial event in dry age-related macular degeneration and gyrate atrophy. The polyamine spermidine has been shown to induce RPE cell death in vitro. The present study aimed to establish a novel in vivo model of spermidine-induced RPE degeneration and to determine whether spermidine-induced RPE cell death involves oxidative mechanisms. In this study, spermidine caused ARPE-19 cell death in a concentration-dependent manner. This effect was prevented by removal of serum from the culture medium or treatment with amine oxidase inhibitors, N-acetylcysteine (NAC), or aldehyde dehydrogenase (ALDH). Intravitreal injection of spermidine into rats significantly increased the permeability of the blood-retinal barrier and decreased the amplitudes of scotopic electroretinogram a- and b-waves. Histological analysis revealed that spermidine induced vacuolation, atrophy, and dropout of RPE cells, leading to the disruption of photoreceptor outer segments. Simultaneous intravitreal administration of NAC and ALDH with spermidine prominently inhibited the functional and morphological changes induced by spermidine. In conclusion, this study demonstrated that the intravitreal administration of spermidine induced RPE cell dysfunction and death followed by photoreceptor degeneration in rats. These effects of spermidine are thought to be mediated by oxidative stress and a toxic aldehyde generated during spermidine oxidation.
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