CINNAMALDEHYDE-INDUCED MICRONUCLEI IN RODENT LIVER

Cinnamaldehyde, a widely used flavoring agent, has so far been subject ed to a limited range of genotoxicity tests, mainly carried out in vit ro, which produced contradictory results. Therefore we have examined c innamaldehyde using additional in vivo genotoxicity end-points. In Spr ague-Dawley rats, a single oral dose equal to 1/2 LD(50) did not induc e DNA fragmentation in liver and gastric mucosa as evaluated by the al kaline elution technique, increased the frequency of micronucleated he patocytes but not of bone marrow micronucleated polychromatic erythroc ytes, and gave rise to a significantly higher incidence of total nucle ar anomalies but not of micronucleated cells in forestomach mucosa. In Swiss mice, the equitoxic dose of cinnamaldehyde caused the same clas togenic effect in the liver, whilst a negative response was observed i n both bone marrow and forestomach mucosa. Finally, in rats initiated with N-nitrosodiethylamine the administration of 500 mg/kg/day cinnama ldehyde for 14 successive days produced a modest but statistically sig nificant increase of the average diameter and area of gamma-glutamyltr anspeptidase-positive foci that, together with changes observed in oth er parameters, might be considered indicative of a potential promoting activity. Taken as a whole, these findings confirm that high doses of cinnamaldehyde may induce genetic alterations at the chromosomal leve l, land suggest that the liver is the preferential target of its undes irable effects.