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Aluminium (Al) is a widespread environmental contaminant known to induce oxidative stress and genotoxic effects in aquatic organisms. While its neurotoxic properties are well-documented, the molecular impact of Al on the visual system remains poorly under-stood. In this study, adult zebrafish (Danio rerio) were exposed to 11 mg/L Al for 10, 15 and 20 days, to investigate the oxidative and genotoxic responses in ocular tissue. Activities of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were measured in eye supernatants to detect oxidative stress. Additionally, the activities of poly(ADP-ribose) polymerase (PARP) and poly(ADP-ribose) glycohydrolase (PARG) were assessed in tissue homogenates to evaluate oxidative DNA damage and repair processes. The results indicate that these enzymes respond to counteract the increased reactive oxy-gen species (ROS) induced by aluminium exposure. However, their activity may not suffi-ciently reduce ROS levels to fully prevent oxidative DNA damage, as evidenced by a sig-nificant rise in PARP activity during short exposure times. Over longer exposures, PARP activity returned to baseline, suggesting ocular cells may adapt to aluminium toxicity. We propose that this reduction in PARP activity is a cellular survival mechanism, as sus-tained activation can deplete energy reserves and trigger cell death. Finally, thin-layer chromatography confirmed that PARG facilitates the breakdown of poly(ADP-ribose) (PAR) into ADP-ribose, demonstrating the dynamic regulation of the PAR cycle, which is crucial to preventing parthanatos.