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Published on: December 20, 2024
Morphologic characteristics of retinal degeneration induced by sodium iodate in mice
Katsuji Kiuchi1, Katsuhiko Yoshizawa, Nobuaki Shikata
1Department of Pathology II, Kansai Medical University, Osaka, Moriguchi, Japan.
Purpose:
Retinal degeneration induced by sodium iodate (NaIO( 3)) in mice was evaluated morphologically.
Methods:
Male and female ICR and C57BL mice were intraperitoneally administered 100 mg/kg NaIO(3) at 7 weeks of age, and were killed 6, 12, 24 hrs, and 3, 7 and 28 days after the treatment. Retinas were examined histologically, ultrastructurally, immunohistochemically, and by the TUNEL method.
Results:
Retinal degeneration was evoked in all NaIO(3)-treated mice. The primary site of damage appeared in the retinal pigment epithelial (RPE) cells followed by photoreceptor cell degeneration. Initially, the RPE cells showed necrosis starting 6 hrs post-NaIO(3), followed by photoreceptor outer segment disruption and photoreceptor cell apoptosis at 24 hrs; photoreceptor cell apoptosis peaked at day 3 and was completed by day 7. At day 3, Müller cell proliferation, macrophage migration within the retina, and regeneration of damaged RPE cells occurred. Finally at day 7 and day 28, the retina showed a mosaic pattern of relatively normal retina and areas lacking RPE cells and photoreceptor cells.
Conclusions:
RPE cell necrosis followed by photoreceptor cell apoptosis and the resulting mosaic pattern of the retina phenotypically resembles gyrate atrophy of the choroid and retina.
Insights
Sodium iodate (NaIO3) induces retinal degeneration in mice, starting with retinal pigment epithelial (RPE) cell necrosis and progressing to photoreceptor cell apoptosis. This results in a mosaic retinal pattern, mimicking gyrate atrophy.
Area of Science:
- Ophthalmology
- Toxicology
- Cell Biology
Background:
- Retinal degeneration is a significant cause of vision loss.
- Understanding the mechanisms of retinal damage is crucial for developing therapeutic strategies.
- Sodium iodate (NaIO3) is a known toxin that can induce retinal damage in experimental models.
Purpose of the Study:
- To morphologically evaluate retinal degeneration induced by sodium iodate (NaIO3) in mice.
- To characterize the temporal sequence of cellular events following NaIO3 administration.
- To investigate the potential of NaIO3-induced retinal damage as a model for human retinal diseases.
Main Methods:
- Male and female ICR and C57BL mice were administered 100 mg/kg NaIO3 intraperitoneally.
- Retinas were examined at various time points (6, 12, 24 hrs, and 3, 7, 28 days) post-treatment.
- Histological, ultrastructural, immunohistochemical, and TUNEL methods were employed.
Main Results:
- NaIO3 induced retinal degeneration in all treated mice.
- Retinal pigment epithelial (RPE) cells showed necrosis starting at 6 hours.
- Photoreceptor cell apoptosis occurred at 24 hours, peaking at day 3 and resolving by day 7.
- Müller cell proliferation and macrophage migration were observed at day 3.
- A mosaic pattern of normal and damaged retina was evident by day 7 and 28.
Conclusions:
- NaIO3-induced retinal degeneration involves RPE cell necrosis followed by photoreceptor cell apoptosis.
- The resulting mosaic retinal pattern shares phenotypic similarities with gyrate atrophy of the choroid and retina.
- This model provides insights into the pathogenesis of certain retinal degenerative diseases.

