The neuropsychiatric conditions; depression and anxiety develop from oxidative stress together with neuroinflammation. The research evaluates if lutein ameliorates anxiety and depression symptoms in rats exposed to scopolamine. 36 male Wistar rats (105g - 153g) were distributed randomly into six distinct groups. Group 1: Negative Control, Group 2: Scopolamine only treated group, Group 3: Scopolamine + Lutein (20mg/kg), Group 4: Scopolamine + Lutein (40mg/kg), Group 5: Scopolamine + Lutein (60mg/kg), Group 6: Scopolamine + Imipramine (standard drug - 10mg/kg). Scopolamine was administered intraperitoneally and lutein orally. Statistical analysis was conducted through one way ANOVA with Post hoc Fischer’s LSD. The experiment used P<0.05 for multiple comparison significance detection. Superoxide Dismutase (SOD), and Glutathione (GSH) levels in Group 2 decreased substantially (p < 0.01 and p < 0.0001) when compared to control, Groups 4, 5, 6 which improved the SOD and GSH levels toward normal levels. Catalase decreased dramatically (p < 0.0001) in Group 2 but treatment in Groups 4 and 5 elevated significantly (p < 0.01). These outcomes establish that Lutein protects against scopolamine induced oxidative stress, behavioral deficits and neurotoxicity. The research established that lutein treatment produced positive results for reversing both oxidative stress conditions and neurotoxicity effects and behavioral deficits provoked by scopolamine. Scopolamine caused a decrease in antioxidant enzymes levels which Lutein treatment at middle and high doses (40 and 60 mg/kg) successfully countered by restoring biomarkers, boosting neurotrophic signals for better behavioral results.