Abstract
Purpose :
Acrolein (Acr) is the simplest unsaturated aldehyde, commonly used as a broad-spectrum biocide for controlling plant growth in water systems and as an intermediate in industrial applications. Given its accessibility and prior use as a chemical weapon in World War I, Acr has been recognized as a chemical of concern. Yet, despite the eyes being highly vulnerable to chemical exposure, there has been limited study on ocular injury resulting from acute Acr exposure. This study applied multimodal imaging to characterize temporal and spatial changes in corneal architecture induced by acute Acr exposure.
Methods :
Following an IACUC-approved protocol, a murine model of chemical burn (n=10) was used to characterize the corneal response to acute topical Acr exposure (2.5 mg/mL for 30 s). Anterior segment optical coherence tomography (AS-OCT), OCT angiography (OCTA), and slit lamp biomicroscopy were performed prior to the injury and up to 28 days following the injury. On day 28, fluorescein angiography (FA) was performed, and eyes were enucleated for histology and qPCR assessment.
Results :
Acr exposure resulted in persistent mild corneal swelling that did not appear to fully recover. Corneal thickness measurements from AS-OCT corroborated this observation, with swelling peaking on day 3 (+21%), remaining plateaued through day 7, before partial recovery occurred. There was a similar trend with changes in corneal opacity measured by OCTA, with opacity peaking on day 3 (+20%). OCTA and FA showed that 80% of the mice were affected by limbal neovascularization, beginning as early as day 14 before spreading centrally. Preliminary histology indicates the possibility of corneal stromal fibroblast loss and the presence of collateral damage beyond the anterior segment.
Conclusions :
We demonstrated that topical exposure of the eye to Acr leads first to only mild corneal swelling before later causing neovascularization. This contrasts the serious pathologies, such as severe corneal edema and Descemet’s membrane detachment, that typically precede the development of neovascularization observed in other chemical eye injury models (e.g., sodium hydroxide, mustard gas). With only mild signs of corneal injury present prior to the onset of neovascularization, we hypothesize that Acr causes an accumulation of protein and DNA damage that leads to cell death, playing an important role in the corneal wound-healing response following Acr exposure.
This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.