Hypercarotenaemia can occur at any age but it is more commonly seen in infants and young childrendue to the excessive intake of carotenoid bearing food. The objective of this study was to inducehypercarotenaemia and trace the fate of excess carotenoids in Wistar rats and ICR mice. Wistarrats (n=20) and ICR mice (n=28) were used. Rats and mice were divided into two groups (Test andControl). The controls were fed with standard rat/mice pellets while test group was fed with freeze-dried carrot incorporated standard rat/mice feed with boiled carrot. After a month and 2.5 months,blood was drawn for analyses of carotenoids and metabolites and after 2.5 months liver, adiposeand digesta of rats were collected. Faeces were freeze dried and then analyzed for carotenoids ofmetabolites (RP-HPLC). Serum, adipose, liver and bile of test and control mice were also analyzedas above.Wistar rats and ICR mice fed on excess carrot and papaw did not show outward signs ofhypercarotenaemia. Their serum, adipose tissue, liver, digesta (in the case of rats) and bile (in thecase of mice) did not show detectable amounts of carotenoids or their metabolites. However thefaeces of both rat and mice had high levels of α and β carotenes. This indicates that one method ofcontrol of hypercarotenaemia may be at the level of absorption.Key words: hypercarotenaemia, Induction of, Wistar rats and ICR mice, papaw, carrot die
