Accelerator mass spectrometry (AMS) is an ultrasensitive analytical technique for measuring rare nuclides such as 14C, 26Al and 41Ca. The low detection limit and wide dynamic range of AMS allow long-term and highly sensitive tracer studies in nutrition that cannot be performed with other methods. The present paper is intended to provide a description of AMS to the interested nutritionist and present proven applications. AMS is compared to liquid scintillation counting and stable isotope MS. A description of common AMS methodology is presented that consists of determining the dose, preparing the sample, diluting the sample (if necessary), and measuring the sample. Applications include Ca metabolism, Al uptake from the environment, dietary intake of carcinogens, fat meta-bolism and folate metabolism. Throughout this discussion the experimental advantages (small doses that pose no health risk, extremely long experimental lifetime, small sample sizes and high sensitivity) made possible by the unique analytical capabilities of AMS are emphasized. The future of AMS is discussed. As the number of AMS centres, instruments, and studies increases, the number of nutritional applications that employ AMS will continue to grow. The coupling of AMS with other analytical techniques (e.g. high performance liquid chromatography) will be developed as access to AMS improves.

The anticarcinogenic effect of vitamin A2 (dehydroretinol and 3-hydroxyretinol) compounds was studied and compared with that of vitamin A1 (retinoic acid, retinol and retinal) and carotenoids (lutein and β-carotene) in the benzo[a]pyrene (B(a)P)-induced forestomach tumour model of female Swiss mice in vivo. Tumour growth and gross tumour incidence observed after the administration of B(a)P (eight doses of 1 mg, twice weekly for 4 weeks) and retinoids/carotenoids (2·5 and 4·7 μm per animal per d, 2 weeks before, during and 2 weeks after B(a)P) showed that the groups supplemented with lutein and 3-hydroxyretinol produced the best results in inhibiting tumour growth and had low tumour incidence compared with the control group given B(a)P only (P<0·05). Weights recorded after the different treatments showed that the β-carotene-supplemented group exhibited maximum weight gain, followed by retinal, retinol, retinoic acid, lutein, dehydroretinol and 3-hydroxyretinol. These results indicate that the anticarcinogenicity of the compounds is not related to the vitamin A biopotencies. Vitamin A2 compounds having half the biopotency of the vitamin A1 compounds were seen to be anticarcinogenic. Again, among the carotenoids, lutein, having 50 % less biopotency, showed more significant results than β-carotene. Thus it is imperative to conclude that the low animal growth achieved with these compounds has a correlation with the highest suppression of tumour occurrence in the present experiment. Therefore, the daily consumption of foods having high content of lutein and vitamin A2 should be given due importance and weight in further studies.