Alterations of glycosaminoglycans synthesized by chick embryo cartilage treated with 6-aminonicotinamide.

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Abstract
Treatment of day-4 chick embryos with 6-aminonicotinamide (6-AN) impairs limb chondrogenesis and produces micromelia. Treatment of day-10 chick embryos with 6-AN does not produce micromelia. Here, the glycosaminoglycan (GAG) biosynthesis in the cartilage isolated from the day-10 chick embryos treated with 6-AN in vitro and in the cartilage from the day-11 chick embryos treated with 6-AN in ovo at day-10 was examined. In the epiphyseal cartilage treated in vitro, the radioactivity incorporated into the GAG fraction was significantly decreased and the 35S/3H ratio in the GAG fraction and the molecular size of GAG chain were also decreased. Percent distribution of .DELTA.Di-OS was almost unchanged. In the epiphyseal and diaphyseal cartilage treated in ovo at day-10, the alteration in GAG biosynthesis was not observed except the reduction of the molecular size of GAG in epiphyseal cartilage. Biosynthetic activity of GAG in the process of recovery/repair was also examined using the micromelial cartilage isolated from day-11 chick embryos given 6-AN in ovo at day-4. In the diaphyseal cartilage, the radioactivity incorporated into the GAG fraction and the 35S/3H ratio were increased; percent distribution of .DELTA.Di-OS was almost unchanged. Treatment of day-4 chick embryos with 6-AN produces the rebound phenomena in the diaphyseal cartilage isolated at day-11. 6-AN directly impairs GAG biosynthesis in epiphyseal cartilage. Effects of 6-AN on isolated cartilage differ from the effects of 6-AN on limb mesoderm in ovo. Thus, the defects induced by 6-AN in isolated cartilage cannot be conceived of as the cause of the bone malformation asserted by Seegmiller et al.