Meso-zeaxanthin was investigated for antimutagenic and anticarcinogenic activity, using the Ames test(Salmonella typhimurium strains TA 98, TA 100, TA 102 and TA 1535) with direct acting mutagens like sodiumazide (NaN3) (5 μg/ plate), nitro-o-phenylendiamin (NPD) (20 μg/ plate), N-methyl- N’-nitro-N-nitrosoguanidine(MNNG) (1μg/ plate) and tobacco extract 50 mg/ plate) and with a mutagen needing microsomal activation,acetamidofluorene (AAF) ( 20 μg/ plate). The carotenoid was found to inhibit the mutagenicity induced byNaN3, NPD and MNNG in a concentration dependent manner, as well as that with AAF and the tobacco extract.Concentrations needed for 50 % inhibiton was found to be 50 μg/ plate for the chemical mutagens and 100 μg/plate for tobacco extract. Using specific resorufin derivatives as substrates in vitro, the concentration of mesozeaxanthinneeded for 50 % inhibition of CYP1A2 (7-methoxyresorufin-O-demethylase) was 5 μg/ml, for CYP2B1/2 (7- pentoxyresorufin-O-depentylase) was 8 μg/ml and for CYP1A1 (7-ethoxyresorufin-O-deethylase) was 12μg/ml, while that of CYP 2E1 (aniline hydroxylase) was 7μg/ml and for CYP 1A, 2A, 2B, 2D and 3A (aminopyrene-N-demethylase) was 10.5 μg/ml. Evaluated using nitroso diethyl amine (NDEA) induced hepatocellular carcinomain rats, treatment with meso-zeaxanthin reduced the tumor incidence when compared to the control group. Theactivity of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and alkaline phosphatase wasdrastically elevated in both serum and liver tissue of NDEA alone treated control animals and meso-Zeaxanthinpretreated animals showed significant decrease to normal levels, in line with histopathological findings.