<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee TT</submitter><funding>NEI NIH HHS</funding><funding>NIH HHS</funding><pagination>110221</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11798707</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>251</volume><pubmed_abstract>Previously, we found that retinas of young male mice were more damaged than those of young female mice in the sodium iodate (NaIO&lt;sub>3&lt;/sub>) model. The purpose of this study was to test whether reducing testosterone levels would be retina-protective. Male C57Bl/6J mice underwent surgical castration or sham surgery, then were given an intraperitoneal injection of NaIO&lt;sub>3&lt;/sub> at 25 mg/kg. The mice were imaged a week later using optical coherence tomography (OCT). ImageJ with a custom macro was utilized to measure retinal thicknesses in OCT images. Electroretinography (ERG) was used to measure retinal function one week post-injection. After euthanasia, quantitative real-time PCR (qRT-PCR) was performed. Surgical castration partially protected photoreceptors, which was indicated by less photoreceptor layer thinning exhibited in OCT images compared to the sham surgery group. Consistent with this, qRT-PCR of castration group neural retinas revealed less reduction of rhodopsin mRNAs, and less upregulation of antioxidant as well as glucose transporter 1 mRNAs. ERG results also demonstrated partial preservation of both cone and rod function. These results indicate that surgical castration provided structural and functional protection to photoreceptors against NaIO&lt;sub>3&lt;/sub>. These neuroprotective effects suggest that testosterone may be harmful to the stressed retina. Further investigation of this pathway could lead to a better understanding of the mechanisms involved in retinal degeneration.</pubmed_abstract><journal>Experimental eye research</journal><pubmed_title>Testosterone promotes photoreceptor degeneration in the sodium iodate model.</pubmed_title><pmcid>PMC11798707</pmcid><funding_grant_id>P30 EY001583</funding_grant_id><funding_grant_id>R01 EY036292</funding_grant_id><funding_grant_id>S10 OD026860</funding_grant_id><funding_grant_id>R01 EY028916</funding_grant_id><funding_grant_id>R01 EY015240</funding_grant_id><pubmed_authors>Bell BA</pubmed_authors><pubmed_authors>Lee TT</pubmed_authors><pubmed_authors>Dunaief JL</pubmed_authors><pubmed_authors>Song Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Testosterone promotes photoreceptor degeneration in the sodium iodate model.</name><description>Previously, we found that retinas of young male mice were more damaged than those of young female mice in the sodium iodate (NaIO&lt;sub>3&lt;/sub>) model. The purpose of this study was to test whether reducing testosterone levels would be retina-protective. Male C57Bl/6J mice underwent surgical castration or sham surgery, then were given an intraperitoneal injection of NaIO&lt;sub>3&lt;/sub> at 25 mg/kg. The mice were imaged a week later using optical coherence tomography (OCT). ImageJ with a custom macro was utilized to measure retinal thicknesses in OCT images. Electroretinography (ERG) was used to measure retinal function one week post-injection. After euthanasia, quantitative real-time PCR (qRT-PCR) was performed. Surgical castration partially protected photoreceptors, which was indicated by less photoreceptor layer thinning exhibited in OCT images compared to the sham surgery group. Consistent with this, qRT-PCR of castration group neural retinas revealed less reduction of rhodopsin mRNAs, and less upregulation of antioxidant as well as glucose transporter 1 mRNAs. ERG results also demonstrated partial preservation of both cone and rod function. These results indicate that surgical castration provided structural and functional protection to photoreceptors against NaIO&lt;sub>3&lt;/sub>. These neuroprotective effects suggest that testosterone may be harmful to the stressed retina. Further investigation of this pathway could lead to a better understanding of the mechanisms involved in retinal degeneration.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2026-06-13T05:28:24.693Z</modification><creation>2026-06-13T03:09:21.263Z</creation></dates><accession>S-EPMC11798707</accession><cross_references><pubmed>39710099</pubmed><doi>10.1016/j.exer.2024.110221</doi></cross_references></HashMap>