In this study, we aimed to explore the changes of oxidative stress, Δ9- tetrahydrocannabinol (Δ9-THC) and its metabolites accumulation in the liver of type-2 diabetic rats treated with Δ9-THC. 8-10 week-old Sprague-Dawley rats were divided into four groups. Group I: Physiological saline was administered intraperitoneally(i.p) (n=7). Group II: Rats that was given Δ9-THC for 7 days (3 mg/kg/day) (n=6) (i.p). Group III: Streptozotocin(STZ, 65 mg/kg)+Nicotinamide(NAD, 85 mg/kg) (n=7) (i.p). Group IV: Diabetic rats that were given Δ9-THC(3 mg/kg/day) for 7 days (n=7) (i.p). The biochemical investigation was carried out on the serum and liver tissue. Δ9 -THC and its metabolites were analyzed by using GC- MS in the liver of rats. Liver glutathione level in diabetes+ Δ9-THC increased as compared to diabetic rats. The increased lipid peroxidation and protein carbonyl levels in diabetes showed a low reduction with Δ9-THC. Catalase and superoxide dismutase activities in liver of diabetic rats increased with Δ9- THC treatment, non-statistically. Serum uric acid level, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities slightly increased in diabetic group as compared to control group. While the AST level reduced in the liver, ALT level did not be affected in Δ9-THC treated with diabetic rats as compared with the diabetic group. Δ9-THC level in liver was negative in given Δ9-THC groups. But the liver THC-COOH metabolite accumulation in Δ9-THC group is higher than Diabetes + Δ9-THC group. We could say that Δ9-THC can reduce diabetes-induced oxidative damage in the liver of type-2 diabetic rats. The metabolization of Δ9-THC in the liver can be accelerated with diabetes.