Cell apoptosis caused by free-radical formation during phacoemulsification can be mediated by the introduction of ascorbic acid, according to a study published in the December 2008 issue of the Journal of Cataract & Refractive Surgery.
Cell apoptosis caused by free-radical formation during phacoemulsification can be mediated by the introduction of ascorbic acid, according to a study published in the December 2008 issue of the Journal of Cataract & Refractive Surgery.
Naphtali Savion, PhD of Tel-Aviv University, Israel and colleagues assessed cell apoptosis in bovine corneal endothelial cells (CECs), which were cultured on gas-permeable flexible membranes, and then exposed to phacoemulsification. As a control, the researchers also examined cell apoptosis in CECs exposed to hydrogen peroxide for a period of 48 hours.
The researchers found that cell apoptosis increased from 45±12 apoptic nuclei per square millimetre before phacoemulsification to 334±29 48 hours postoperatively. Following 48 hours' exposure to hydrogen peroxide, apoptosis was 345±6 (H2O2 concentration, 50 µM) and 376±1 (H2O2 concentration, 100 µM). Adding ascorbic acid decreased the mean 48-hour post-phaco apoptosis level to 219±15 (ascorbic acid concentration, 1 mM) and 130±29 (ascorbic acid concentration, 10 mM), although applying shear forces up to 2000 seconds1 for 60 minutes did not alter the rate of apoptosis.
The researchers concluded that the increased rate of cell apoptosis that results from phacoemulsification is likely to be caused by free radical formation, and can therefore be modified through the application of ascorbic acid.