Liver growth retardation in corticosteroid-treated neonatal mice.
This study examined the influence of triamcinolone hexacetonide on the growth and nucleic acid synthesis in the liver of neonatal mice. Following a single dose of the hormone the synthesis of DNA was significantly depressed, a feature that lasted for 72 hours. Thereafter an almost full recovery took place and by 144 hours no significant differences existed between hormone-treated livers and their nontreated controls. The above inhibitory effect was dose-dependent and was specific to steroids with glucocorticoid activity. A markedly different response was noted in regard to RNA synthesis. Hormone-treated livers revealed an initial increase in the uptake of 3H-uridine and RNa synthesis but later on revealed a significant decrease in the incorporation of uridine resulting in a marked reduction in the tissue's content of RNA. Concomitantly, the hormone increased significantly the protein content of the liver. It thus became clear that glucocorticoid hormones possess both a significant inhibitory effect upon the proliferative activity of neonatal hepatocytes and interfere with the latters' protein synthetic machinery, thereby affecting the normal growth of the liver at its critical period of growth and development.
D000818:Animals; D000831:Animals, Newborn; D004247:DNA / Q000096:biosynthesis*; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D008099:Liver / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D008297:Male; D051379:Mice; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis*; D014222:Triamcinolone Acetonide / Q000031:analogs & derivatives* / Q000494:pharmacology
D012313:RNA; D003907:Dexamethasone; D004247:DNA; D014222:Triamcinolone Acetonide; C005900:triamcinolone hexacetonide