Alterations of Bioactive Lipid Profiles in the Retina Following Traumatic Optic Neuropathy in Mice

Document Type

Article

Publication Date

10-14-2025

Publication Title

Biomolecules

Abstract

Traumatic optic neuropathy (TON) causes vision loss through compression and contusion, yet there is no consensus on the most effective treatment. Polyunsaturated fatty acid (PUFA)-derived bioactive lipids metabolized by lipoxygenase (LOX), cytochrome P450 (CYP), and cyclooxygenase (COX) enzymes are known mediators of inflammation and neurodegeneration. However, their role in TON-related retinal pathology remains unclear. Controlled orbital impact (COI) was used to induce unilateral TON in mice with controlled velocity (2-3 m/s), with the fellow eye serving as an internal control. Retina tissues were collected three days post-injury and analyzed by LC/MS to quantify bioactive lipid metabolites from ω-6 and ω-3 PUFAs. Statistical analysis was performed using paired, nonparametric Wilcoxon signed-rank tests with Benjamini-Hochberg false discovery rate (FDR) correction. Results showed that among 38 reliably detected metabolites, no individual lipid showed a statistically significant difference between TON and control eyes after FDR correction (q < 0.05). However, both individual and pathway-level analysis revealed consistent trends toward increased expression of LOX- and CYP-derived metabolites across FDA PUFA substrates, including arachidonic acid (AA), linoleic acid (LA), and docosahexaenoic acid (DHA). These findings support further investigation into lipid-mediated inflammation in TON and its potential as a therapeutic target, particularly through expanding both the sample size and the post-TON time periods.

Volume

15

Issue

10

DOI

10.3390/biom15101450

ISSN

2218-273X

PubMed ID

41154681

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