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
sodium azide (
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 by
NaN3,
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
meso-zeaxanthin needed for 50 % inhibition of
CYP1A2 (7-
methoxyresorufin-O-demethylase) was 5 µg/ml, for CYP2B 1/2 (7-
pentoxyresorufin-O-depentylase) was 8 µg/ml and for
CYP1A1 (7-
ethoxyresorufin-O-deethylase) was 12 µg/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 carcinoma in rats, treatment with
meso-zeaxanthin reduced the
tumor incidence when compared to the control group. The activity of
glutamate oxaloacetate transaminase,
glutamate pyruvate transaminase and
alkaline phosphatase was drastically elevated in both serum and liver tissue of NDEA alone treated control animals and
meso-Zeaxanthin pretreated animals showed significant decrease to normal levels, in line with histopathological findings.