Reactive metabolites produced during the metabolism of drugs or toxic substances can cause hepatocellular damage, and drug-induced liver injury (DILI) is a major cause of acute liver failure. In this study, the liver protective effect and mechanism of pectin were investigated using a CCl₄-induced mouse model. Male ICR mice were supplied with 2.5% or 5% pectin for 2 weeks prior to CCl₄ (0.52 mmol/kg equivalent to 79.5 mg/kg). CCl₄ administration resulted in an increase in serum ALT and AST activity, induction of hepatic lipid accumulation, oxidative stress, decreased CYP expression and disruption of SAA metabolism. On the other hand, pectin supplementation restored histological liver damage and SAA metabolism to increase cysteine supply, which led to the promotion of GSH synthesis in the liver. Increased GSH relieved oxidative stress by increasing the activity of antioxidant enzymes such as GR, GPx1 and GST-α.  These results suggest that pectin acts as a dietary bioactive agent that protects the liver and maintains liver health by mitigating oxidative damage through the interconnection between sulfur amino acid metabolic recovery and GSH-dependent antioxidant defense enhancement.