The liver is one of the primary biorepositories of cadmium and it has been implicated in the pathogenesis of hepatic diseases [1,2]. In this study, cadmium was administered to rats to induce hepatic oxidative damage and derangement of lipid panel. The effects of Quassia amara on these markers in cadmium treated rats were thereafter examined. Rats were divided into 3 groups. Group 1 served as control, Group 2 received cadmium (5 mg/kg) for 4 weeks while Group 3 was pre-treated with Q. amara extract (200 mg/kg) for 2 weeks and received Q. amara and cadmium concurrently for another 4 weeks. Rats were sacrificed 24 hours after the last treatment by cervical dislocation under sodium pentobarbital (30 mg/kg IP) anesthesia and blood samples were obtained by cardiac puncture. Lipid profile was assayed by colorimetric method from serum obtained while hepatic oxidative stress was assayed spectrophotometrically from liver homogenate using respective commercial available kits [3]. All procedures in this study conformed to the guiding principles for research involving animals as recommended by the Declaration of Helsinki and the Guiding principles in the care and Use of animals (2002). Cadmium caused significant increase in serum cholesterol (152.96 ± 13.98 vs 123.86 ± 9.61 mg/dl) and LDL (102.17 ± 8.08 vs 86.85 ± 6.31 mg/dl) and decreased HDL (3.01 ± 0.40 vs 5.65 ± 1.02 mg/dl) when compared with control. Also, hepatic MDA was higher (12.75±2.3 vs 4.27±0.56 iµ/ml) while SOD (0.25±0.04 vs 0.87±0.16 iµ/ml) was lower in cadmium treated rats compared with the control. However, Q. amara prevented cadmium-induced increase in cholesterol (123.83 ± 9.41 vs 152.96 ± 13.98 mg/dl) and LDL (84.53 ± 4.31 vs 102.17 ± 8.08 mg/dl) and prevented cadmium-induced decrease in HDL (6.66 ± 0.91 vs 3.01 ± 0.40 mg/dl). Also Q. amara augmented cadmium-induced decline in SOD (0.62±0.13 vs 0.25±0.04 iµ/ml) and ameliorated cadmium-induced increase in MDA (6.16±0.87 vs 12.75±2.3). In conclusion, Quassia amara stem bark has hepatoprotective properties as it ameliorated cadmium-induced damage to liver by preventing dyslipidemia and oxidative damage in the hepatic tissue.