Ethanol (EtOH) intake and noise exposure are particularly concerning among human adolescents because the potential to harm brain. Unfortunately, putative underlying mechanisms remain to be elucidated. Moreover, although neuroprotection tools could aid to prevent individuals from injury, limited data are available. Using an adolescent animal model, present study aims to explore a possible mechanism that could underlie the altered hippocampus-dependent behaviors induced by EtOH intake and/or noise exposure, as well as the neuroprotective impact of an environmental challenge. Adolescent Wistar rats of both sexes were subjected to an intermittent voluntary EtOH intake paradigm for one week. A subgroup of animals was exposed to white noise for two hours after the last session of EtOH intake. Some animals of both groups were housed in EE cages. Hippocampal-dependent behavioral assessment and hippocampal oxidative state evaluation were performed. Present results show that different behavioral alterations might be induced in animals of both sexes after EtOH intake, with or without sequential exposure to noise, that in some cases are sex-specific. Moreover, hippocampal oxidative imbalance seems to be one of the potential underlying mechanisms. Additionally, most behavioral and oxidative alterations were prevented by EE. These findings suggest that two recreational agents may impact behavior via oxidative pathways, in both sexes, in an animal model. In addition, improved housing resulted an effective neuroprotective strategy. Therefore, it could be suggested that a non-pharmacological approach might potentially provide neuroprotective advantages against other challenges. Finally, it might be worth considering its potential for translational human benefit.