Introductıon The aim of this study was to investigate the protective effects of apocynin in a selenite-induced cataract model, and to evaluate its impact on cataract severity and antioxidant enzyme activities. Given the limited availability of pharmacological strategies to delay cataract progression, the identification of agents that modulate oxidative stress may provide translational insight for the development of future non-surgical approaches. Methods In this randomized experimental study, thirty-five rats were randomly separated into five groups (n = 7 per group). The control group received only saline. Groups 1, 2, 3, and 4 were administered sodium selenite at a dose of 30 nmol/g. In addition, Group 2 received dimethyl sulfoxide (DMSO), Group 3 received 10 mg/kg apocynin, and Group 4 received 20 mg/kg apocynin. The apocynin treatment was administered intraperitoneally for 7 consecutive days. Cataract severity was defined as the primary outcome, while antioxidant enzyme activities and oxidative stress markers were evaluated as secondary outcomes. Results Low-dose apocynin was seen to enhance antioxidant defence by increasing catalase (CAT) and glutathione reductase (GR) levels (p = 0.003, p = 0.002) without altering malondialdehyde (MDA) levels (p = 0.04). High-dose apocynin (20 mg/kg) led to an increase in MDA, suggesting a possible dose-related pro-oxidant effect. Conclusion This study suggests that apocynin, particularly at a low dose (10 mg/kg), may prevent selenite-induced cataract formation. Low-dose apocynin effectively delayed cataract progression by enhancing antioxidant defence and limiting oxidative stress. In contrast, high-dose exposure revealed a possible pro-oxidant effect, highlighting the need for careful dose optimization.
Okşar et al. (Sat,) studied this question.