Abstract
Purpose :
We previously reported that cigarette smoke (CS) exposure triggers the loss of corneal endothelial cells (CECs) and disruption of Descemet’s membrane (DM) proteins in mice. Here, we extend our analyses to investigate the changes in the corneal endothelium (CE) and DM exposed to CS in rabbits.
Methods :
The New Zealand White female rabbits weighing approximately 1½ kg were placed in a whole-body exposure smoking chamber for six months. The smoke chamber contained a TE-10 smoking machine and the rabbits were exposed to CS for 5 hours/day, 5 days/week. In parallel, age-, and body weight-matched female rabbits were housed in the animal facility to serve as a control. The CE of CS-exposed and control rabbits were examined using a CEM-530 specular microscope. The rabbits were euthanized post-CS exposure, and the central cornea was examined by a Thermo-Fisher Talos L120C transmission electron microscope for ultrastructure analysis.
Results :
The CEM-530 specular microscope images of CS-exposed and Ct rabbits revealed a difference in the shape of CECs accompanied by a nearly 20% decrease in CEC density following CS exposure. The ultrastructure analysis showed abnormal morphology of CE cells along with extensive vacuolization while the Ct rabbit CE cells revealed normal morphological features. Importantly, mitochondria in the CS-exposed CE cells appeared swollen in comparison with the Ct rabbit cornea. Moreover, the retention of adhesion of CE on DM was affected in CS-exposed rabbits as a result of CS exposure. Further, CS exposure resulted in an increase in the thickness of the DM as compared to Ct rabbits.
Conclusions :
These data suggest that exposure to CS results in reduced CEC density accompanied by disrupted ultrastructure confirming chronic CS exposure-induced damage to the CE and the DM in line with previously published results.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.