Actinomycin D Inhibition of Vitamin D- and Dihydrotachysterol-induced Responses in the Chick

Abstract

Low doses of actinomycin D (2.0–2.5 µg/day for 14 days) administered intraperitoneally to chicks fed a rachitogenic diet did not cause any measurable deterioration of their rachitic state as assessed by serum calcium and phosphorus levels, percentage bone ash, growth, or bone weights. These observations suggest that there is a basal level of intestinal function and bone metabolism in rachitic chicks which is not inhibited by actinomycin D. The increased intestinal absorption of calcium above the basal level induced by oral antirachitic doses (2.5 µg/day) of vitamin D3 or dihydrotachysterol2 (DHT2) was abolished by the above doses of actinomycin D. Bone ash values, however, were normal despite the actinomycin D treatment, although growth was retarded. Actinomycin D reduced the hyperstimulated calcium absorption and lowered the hypercalcemia evoked by the high dosages of vitamin D3 or DHT2 (250 µg/day). Various evidence suggests that certain bone effects of the sterols were relatively unaffected by actinomycin D. In birds receiving 2500 µg/day of vitamin D3, oral 45Ca was well absorbed into the blood but failed to deposit in bone; actinomycin D by inhibiting calcium absorption, caused a lowering of the hypercalcemia, but since bone uptake was negligible, the resultant serum calcium level was not as low as rachitic levels.