Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Wong, Ming D.; Thomson, Marnie J.; Burton, A.F.

doi:10.1159/000240799

Cited by 8 publications

(4 citation statements)

References 1 publication

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“…Subsequent weight gain over the next 42 days was not different from controls. A second injection of dexamethasone was found to be invariably fatal to all fetuses of this strain (10). A single injection, however, caused no increase in fetal deaths in 62 litters.…”

Section: Discussionmentioning

confidence: 76%

Effects of Dexamethasone on Fetal Mouse Development

Tye¹,

Burton²

1980

Neonatology

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The in vitro incorporation of ¹⁴C-leucine, ³H-uridine and ³H-thymidine into the acid-insoluble components of mouse fetal liver, gut, heart and lung was followed on gestational days 14, 16 and 19. Liver and gut showed a similar pattern: the incorporation of all three substrates decreased steadily until day 19, falling from one tenth to one fifth the values on day 14. Heart and lung decreased by half after day 16. Injection of mothers 16 h earlier with 200 μg dexamethasone decreased in vitro incorporation on day 14 into liver and gut, respectively, of leucine by 38 and 37% and of thymidine by 67 and 56%. In heart and lung, only thymidine was decreased at this time by 61 and 33%, respectively. Values for uridine were affected significantly only in liver. Thymidine incorporation appeared to be the most sensitive parameter reflecting corticosteroid action and liver the most sensitive tissue. Treated fetuses were born at the usual time and weight gain did not differ from controls over the first 42 days neonatally. It is concluded that dexamethasone accelerates the development of many processes in fetal tissues which are induced by corticosteroids.

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Section: Discussionmentioning

confidence: 76%

Effects of Dexamethasone on Fetal Mouse Development

Tye¹,

Burton²

1980

Neonatology

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“…That this event is in fact attributable to a change in steroid level is indicated by the fact that injection of dexamethasone on gestational day 13.5 resulted in values on day 14 which were normally found between days 15 and 18 ( Table 2). The synthetic steroid was used here because it largely escapes the normal regulatory mechanisms which protect the fetus from maternal corticosteroids, with the result that a more effective dose reaches the fetus (14).…”

Section: Discussionmentioning

confidence: 99%

Corticosterone Metabolism and the Incorporation of Leucine, Uridine, and Thymidine into Fetal Mouse Brain

1978

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“…The low effectiveness of administered natural 1977 glucocorticoids in utero as opposed to tissue culture is explicable by their rapid metabolism. For example, when radioactive glucocorticoids were injected maternally, the ratio foetal tissue/maternal plasma radioactivity for corticosterone was one-fifth that for dexamethasone; moreover, the ratio of unmetabolized to metabolized steroid per g of foetal tissue was, for corticosterone, some 10 % of that for dexamethasone (Wong et al, 1976). Progesterone had no effect on transferase activity in cultured foetal liver ; its minor stimulation on injection, if real, could be attributed to its metabolism to glucocorticoids.…”

Section: Discussionmentioning

confidence: 97%

“…Because of its persistence in vivo (see Bush et al, 1968;Wong et al, 1976), dexamethasone was preferentially used in the present studies. It was injected (300,ug) into pregnant rats successively on days 14, 15 and 16 of gestation.…”

Section: Methasonementioning

confidence: 99%

Regulation of onset of development of UDP-glucuronosyltransferase activity towards o-aminophenol by glucocorticoids in late-foetal rat liver in utero

Wishart¹,

Dutton²

1977

Biochemical Journal

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1. A precocious development of UDP-glucuronosyltransferase activity (EC 2.4.1.17) towards o-aminophenol is demonstrated in 15-17 day foetal rat liver in utero after dexamethasone administration to the mother. 2. This stimulation of liver transferase activity in utero is directly proportional to the dose of dexamethasone infected. 3. Precocious development of transferase activity in utero can also be effected with the natural glucocorticoid cortisol by multiple injections of large amounts of this hormone into the mother. 4. Transferase activity towards o-aminophenolin foetal lung, kidney and upper alimentary tract can also be precociously stimulated by dexamethasone in 17-day foetuses in utero. 5. Natural development of hepatic transferase activity between days 18 and 20 of gestation is retarded after foetal hypophysectomy by decapitation in utero. 6. Overall glucuronidation of o-aminophenol, as observed in foetal rat liver, is also precociously stimulated by dexamethasone. 7. From this and from evidence previously presented we suggest that glucocorticoids, which are known to increase in rat foetuses between days 17 and 20 of gestation, trigger the normal development in utero of hepatic transferase activity towards o-aminophenol which occurs at that time. We also suggest that these hormones are responsible for the rise in activity of the enzyme in foetal lung, kidney and upper alimentary tract which occurs during the same gestational period.

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Metabolism of Natural and Synthetic Corticosteroids in Relation to their Effects on Mouse Fetuses

Cited by 8 publications

References 1 publication

Effects of Dexamethasone on Fetal Mouse Development

Effects of Dexamethasone on Fetal Mouse Development

Corticosterone Metabolism and the Incorporation of Leucine, Uridine, and Thymidine into Fetal Mouse Brain

Regulation of onset of development of UDP-glucuronosyltransferase activity towards o-aminophenol by glucocorticoids in late-foetal rat liver in utero

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