Fetal Decapitation Research Articles

Gestational Effects of Fetal Decapitation in Sheep

Gestational Effects of Fetal Decapitation in Sheep

Induction of Tyrosine-α-Ketoglutarate Transaminase in Fetal Rat Liver

Abstract Decapitation of fetuses in utero rendered rat liver tyrosine transaminase (l-tyrosine:2-oxoglutarate aminotransferase, EC 2.6.1.5) occasionally inducible by hydrocortisone. By placing fetal rat liver in organ culture, reproducible induction by the steroid could be obtained. Histological and biochemical studies supported the conclusion that the hepatocytes remained healthy over a 3-day period in culture. The response to hormone was very low in fresh explants for the first 12 hours, but thereafter a 4- to 8-fold elevation in enzyme activity was obtained within 4 to 6 hours. The induced level of the transaminase was maintained unless steroid was removed, and then the activity fell rapidly back toward the control level. The optimal effective concentration of hydrocortisone was 10-6 m, but levels as low as 10-8 m produced a limited response. Only the glucocorticoids and the protein hormones insulin and glucagon were active inducers among a number of hormones tested. Cycloheximide and actinomycin D prevented enzyme induction, but hydrocortisone did not affect either general RNA or protein synthesis. Lactic dehydrogenase activity in explants of fetal liver was unaffected by hydrocortisone. Titrations against antibody showed that the tyrosine transaminases in fetal and adult liver are immunologically identical and proved that the increase in enzyme activity in explants exposed to hydrocortisone was due to an increase in enzyme protein. Immunochemical labeling experiments confirmed that synthesis de novo of enzyme protein is stimulated by hydrocortisone. The results are consistent with the hypothesis that the synthesis of this enzyme is repressed during gestation.

Norepinephrine methylation in fetal rat adrenals.

The activity of phenylethanolamine-N-methyl transferase, the enzyme that methylates norepinephrine to form epinephrine, increases rapidly in the fetal rat adrenal during the day preceding epinephrine accumulation. The developmental increase in enzyme activity and the accumulation of epinephrine are prevented by fetal hypophysectomy (decapitation). Administration of adrenocorticotrophic hormone or cortisol acetate largely reverses the effect of fetal decapitation.

Signification de l'“atrophie” des surrénales foetales du rat provoquée par l'hypophysectomie (décapitation)

It has long been recognized that in decapitated fetuses the earlier the pituitary is removed the greater is the reduction in fetal adrenal cortex observed at term. In interpreting such a result two kinds of factors should be considered. (1) a longer period of pituitary deprivation might permit a more pronounced involution of the adrenals; (2) since the adrenals are all the more embryonic when the pituitary is removed earlier, conspicuous differences could be expected to be found at term if the adrenals just more or less retained their initial condition. Growth and differentiation of the adrenals was studied after decapitation of rat fetuses at various stages. In fetuses decapitated on day 16 1 2 , the weight of the adrenals increases until day 21 1 2 , but much less than in controls (Fig. 2). In those decapitated at 17 1 2 days of age, an increase in adrenal weight occurs the next day, and in those decapitated at 18 1 2 days a slight decrease is noticed. In the three groups of animals the adrenals attain on day 21 1 2 a weight corresponding to the value for a normal 18-day-old fetus. In fetuses decapitated on day 19 1 2 the weight of the adrenals decreases only slightly; it essentially maintains the gain acquired during the previous day. Results are expressed as relative weight of adrenals to body weight in Fig. 3 or as percentage in adrenal weight increase or loss in Fig. 4. The cells of the adrenal cortex undergo an actual involution, characterized by a volume decrease (Fig. 6). This decrease in cellular size can be compensated for by cell proliferation to such an extent that the weight of the gland still increases (decapitation at 17 1 2 days). The well known “atrophy” of the adrenals in decapitated rat fetuses results actually from a special mode of development in the absence of the pituitary. These observations have been correlated with the effects of the fetal adrenals on hepatic glycogen deposition.