Abstract
The biochemical effect of a nicotinamide analogue, 6-aminonicotinamide (6-AN), on developing chick embryonic femur was studied. Growth of femur from 9-day-old embryos that had been exposed to 6-AN for 5 days in ovo was not stimulated by PTH in an in vitro culture system. PTH caused a much smaller increase in the cyclic-AMP content in 6-AN-treated femur than in control femur. However, dibutyryl cyclic-AMP stimulated growth of 6-AN-treated femur. A defect in response of 6-AN-treated femur to the growth stimulating action of PTH may explain the production of micromelia by 6-AN.
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