Male rats were administered one of three biodiesels - soy oil methyl ester (SoME-2), canola oil methyl ester (CaME-2), and methyl ester of animal frying oil (FrAME-1) at 5, 50 and 500 mg/kg, or ultra-low sulphur diesel (ULSD) at 500 mg/kg. Control was administered the vehicle (corn oil) only. After 4-week treatment, serum methanol and formic acid were unchanged or minimally elevated in all treatment groups. Mild histopathological changes in the liver were observed in animals receiving 500 mg/kg biodiesels and ULSD but hepatomegaly, increased phase I and II drug-metabolizing enzyme activities and urinary ascorbic acid were found only in the ULSD group. The ULSD group had increased kidney weight, changes in kidney histopathology, and increased urinary albumin and N-acetylgluocosaminidase activity. Biodiesels and ULSD caused increase in hepatic acyl-CoA oxidase activity. ULSD and FrAME-1 caused decrease in serum free fatty acid while CaME-2 caused decreases in both serum triglycerides and free fatty acids. FrAME-1 produced an increase in liver protein carbonyls and ULSD caused increased liver glutathione. The results indicated that ULSD caused more histopathological and biochemical effects than biodiesels. Biodiesels produced lipid effects and oxidative stress that were feedstock-dependent. The mechanisms and significance of increased hepatic acyl-CoA oxidase activity required further study.