Dietary α-carotene is present in oranges and purple-orange carrots. Upon the central cleavage of α-carotene in the intestine, α-retinal and retinal are formed and reduced to α-retinol (αR) and retinol. Previous reports have suggested that αR has 2 % biopotency of all-trans-retinyl acetate due in part to its inability to bind to the retinol-binding protein. In the present work, we carried out three studies. Study 1 re-determined αR's biopotency compared with retinol and 3,4-didehydroretinol in a growth assay. Weanling rats (n 40) were fed a vitamin A-deficient diet for 8 weeks, divided into four treatment groups (n 10/group) and orally dosed with 50 nmol/d retinyl acetate (14·3 μg retinol), α-retinyl acetate (143 μg αR), 3,4-didehydroretinyl acetate (14·2 μg DR) or cottonseed oil (negative control). Supplementation was continued until the control rats exhibited deficiency signs 5 weeks after the start of supplementation. Body weights and AUC values for growth response revealed that αR and DR had 40–50 and 120–130 % bioactivity, respectively, compared with retinol. In study 2, the influence of αR on liver ROH storage was investigated. The rats (n 40) received 70 nmol retinyl acetate and 0, 17·5, 35 or 70 nmol α-retinyl acetate daily for 3 weeks. Although liver retinol concentrations differed among the groups, αR did not appreciably interfere with retinol storage. In study 3, the accumulation and disappearance of αR over time and potential liver pathology were determined. The rats (n 15) were fed 3·5 μmol/d α-retinyl acetate for 21 d and the groups were killed at 1-, 2- and 3-week intervals. No liver toxicity was observed. In conclusion, αR and didehydroretinol are more biopotent than previously reported at sustained equimolar dosing of 50 nmol/d, which is an amount of retinol known to keep rats in vitamin A balance.