The working hypothesis was that treatment of heifers with 17beta-oestradiol (E2) during specific periods of prepuberty would reduce the response of the hypothalamic-pituitary axis to E2 negative feedback and induce an earlier onset of puberty. The effects of chronic treatment with exogenous E2 administered at specific maturational phases on the age and weight at puberty were studied in 96 prepubertal Brahman (3/4-7/8 Bos indicus) heifers (187.0 +/- 3.3 days of age, mean +/- SEM), weighing 149.9 +/- 2.5 kg. Heifers were randomly assigned to one of six groups (n = 16 per group). Groups 2-6 received E2 implants (Compudose 200) for 90-day periods starting at 10, 13, 16, 19 and 22 months of age, while animals in group 1 remained untreated. Implants were placed subcutaneously at the base of the ear. Blood was collected for progesterone (P4) determination by radioimmunoassay (RIA) and the animals were weighed at monthly intervals from 6 to 15 months then weekly from 15 to 28 months of age. Puberty was defined by concentrations of P > 1 ng/ml in plasma and identification of a corpus luteum (CL) by transrectal ultrasonography (Aloka 210DX:7.5 MHZ probe). Treatment with exogenous E2 at any of the ages/treatment intervals evaluated in this study did not reduce age or weight at puberty (P > 0.7). The mean age and weight at puberty of control heifers was 735.3 +/- 19.7 days (range: 597-861) and 299.2 +/- 10.2 kg (range: 233-382), respectively, which is greater than the age and weight at puberty of 481 days and 246 kg, that was previously reported for B. indicus heifers [Post, T.B., Reich, M.M., 1980. Puberty in tropical breeds of heifers as monitored by plasmaprogesterone. Proceedings of the Australian Society of Animal Production 13, 61-62.]. The large variation in age and weight at puberty that was observed in the present study among heifers might indicate an individual animal effect to E2 treatment among some of the treated animals. The lengthy interval from birth to puberty observed in this study, as compared to other studies, reflects the effects of other factors such as genotype, environmental or nutritional influences on puberty.