Biological Science: Research Developments and Innovations Vol. 1

Arsenic (As) is an environmental pollutant associated with hepatic oxidative injury and possible immune-related effects at high doses. This in vivo study evaluated acute arsenic-induced hepatotoxicity and the accompanying pro-inflammatory cytokine response in laboratory rats. Eighteen adult male rats were divided into three groups (n = 6/group). The control group (CON) received no treatment, whereas the remaining groups received a single oral dose of sodium arsenite (13 mg/kg). Animals were sacrificed 1 day and 7 days after exposure and were designated as AS-1 and AS-7, respectively. Serum was collected for biochemical assessment of hepatic enzymes and cytokines, while liver tissue was examined for oxidative stress markers and histopathological changes. Compared with untreated rats, arsenic exposure increased hepatic malondialdehyde levels and reduced total antioxidant levels. Serum concentrations of hepatic enzymes and pro-inflammatory cytokines, including TNF-α, IL-1β and IL-6, also increased significantly in a time-dependent manner compared with control rats. Histopathological examination supported the biochemical findings, showing liver tissue alterations after sodium arsenite exposure, including changes consistent with hepatocyte injury. Overall, the findings indicate that arsenic-induced hepatotoxicity in this rat model is associated with oxidative imbalance and increased pro-inflammatory cytokine responses, with greater effects observed over time. These results provide experimental evidence linking acute arsenic exposure with hepatic inflammatory activation.