Abstract
Purpose :
N-acetylcysteine (NAC) is an amino acid that exhibits antioxidant properties. In this study, we aim to clarify the effects of (R)-N-acetylcysteine amide (NACA) with enhanced tissue permeability and antioxidant capacity on oxidative stress-induced cataract inhibition and antioxidant pathways in lens epithelial cells (LECs).
Methods :
Lenses obtained from 12-week-old Sprague-Dawley Rats were organ cultured with H2O2 (200 μM) and NACA (200 μM) in Medium199. 24 hours later, lens photos were taken under a dark-field stereomicroscope. Mouse LECs (MLECs) were cultured in Dulbecco's Modified Eagle Medium with H2O2 (50-75 μM) ± NACA (100-200 μM). Changes in cell viability were measured by the MTS assay. Expression of Peroxideroxin (Prdx) 6 and Catalase, which are endogenous antioxidant proteins in the lens, were measured by real-time RT qPCR. One-way ANOVA was used for statistical analysis.
Results :
The addition of NACA significantly inhibited H2O2-induced cataracts in vitro (p<0.001) and significantly reduced cell viability of LECs induced by 100μM H2O2 (p<0.001). H2O2 (50-75μM) increased the expression of Prdx6 and Catalase mRNA, but treatment with 100μM NACA significantly suppressed their expressions (p<0.001).
Conclusions :
NACA, as a ROS scavenger, protects LECs by scavenging oxidative stress and inhibiting cataracts. On the other hand, NACA-induced ROS suppression may induce the suppression of the endogenous antioxidant mechanism by over-suppression of ROS in the lens; therefore, we believe that careful attention should be paid to the dosage and timing of NACA administration.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.