Cadmium, a toxic heavy metal and major environmental pollutant, is known for inducing oxidative damage in various organs, including the liver. This study was conducted to evaluate the protective effects of vitamin C against cadmium-induced oxidative liver damage in albino mice. Forty male mice were randomly divided into four groups of ten each. Group 1 served as the control and received a normal diet. Group 2 was treated with vitamin C (1 g/L ascorbic acid in drinking water). Group 3 received cadmium chloride (200 mg/L in drinking water), while Group 4 was exposed to cadmium chloride (200 mg/L in drinking water) along with vitamin C (1 g/L ascorbic acid in drinking water). Exposure to cadmium in mice led to a significant reduction in body weight and an increase in liver weight compared to the control group. Cadmium treatment resulted in elevated levels of glucose, cholesterol, triglycerides, total lipids, bilirubin, and malondialdehyde (MDA), along with increased activities of glutamate-pyruvate transaminase (GPT), glutamic-oxaloacetic transaminase (GOT), and alkaline phosphatase (ALP). Conversely, serum total protein levels, liver reduced glutathione (GSH), and catalase activities were markedly decreased. In conclusion, the present study revealed that cadmium exposure exerts toxic effects on various biochemical and oxidative stress parameters. However, vitamin C supplementation significantly improved these parameters, highlighting its potential as a potent antioxidant. Vitamin C effectively mitigated the oxidative severity of cadmium induced hepatotoxicity, likely through its ability to neutralize reactive oxygen species and enhance antioxidant defense mechanisms