Abstract: Cisplatin (CP) is an effective antineoplastic agent whose clinical application is constrained by organ toxicities, including liver injury. Although the underlying mechanisms of CP-associated hepatotoxicity have been widely explored, the characteristics of early biochemical and molecular responses following acute exposure remain incompletely defined. The present study aimed to examine early alterations in oxidative stress, inflammatory response, and apoptosis-related pathways following acute CP exposure and to evaluate their potential relevance for subsequent hepatotoxic progression. In this study, early alterations in oxidative balance, inflammatory mediators, and apoptosis-related proteins were examined in rat liver tissue after single-dose CP administration at 5, 7.5, and 12 mg/kg. Liver samples collected 3 days post-treatment were analyzed using ELISA-based assays, routine biochemical methods, and Western blotting for Bax and Bcl-2 expression. The results indicated a dose-related disruption of redox homeostasis, evidenced by elevated lipid peroxidation markers and reduced antioxidant activity. In parallel, pro-inflammatory cytokines showed an increasing trend across treatment groups. Apoptotic signaling was also affected, with enhanced Bax expression and reduced Bcl-2 levels, particularly at higher doses. These molecular findings were accompanied by increases in liver-associated enzyme activities. Overall, the data suggest that acute CP exposure induces measurable early changes at the biochemical and molecular levels in hepatic tissue. These alterations may represent initial responses associated with the development of hepatotoxicity. However, further studies incorporating extended observation periods and structural analyses are needed to better define the temporal progression and mechanistic relevance of these findings.