To study the 'in vivo' importance of vitamin D on the natural killer (NK) activity, rats were submitted to privational rickets induced by a diet deficient in vitamin D and phosphorus (D-P-). Thirty days after the beginning of treatment the animals showed low body weight, changes in the bone development, and decreased levels of 25-hydroxyvitamin D(3) (25-OH D(3)). NK activity, evaluated using a cytotoxicity assay against 51Cr-labeled Yac.1 target cells, was not modified by the rickets-inducing treatment during the first 30 days. Following a long-term treatment (60 days) the rachitic rats (D-P-) exhibited higher NK activity than control animals (D+P+) (P<0.05). On the other hand, D-P+ animals showed higher cytotoxic activity than D-P- and D+P+ groups. Feed replacement to the rachitic rats by a complete diet (D-P-/D+P+) led to a partial recuperation of growth, bone development, and 25-OH D(3) serum levels. The NK activity was also influenced by vitamin D intake, decreasing after treatment.