Postnatal Induction Research Articles

Induction of mitosis in the differentiating Purkinje cells of the cerebellum.

The neonate rats of 5 days postnatal age were exposed to low-level X-ray irradiation or were administered microquantities of N-ethyl-N-nitrosourea directly into the cerebellum. Following the initial phase of cell degeneration and phagocytosis of the debris, the surviving Purkinje cells showed recovery of their differentiation. During this stage some Purkinje cells were observed to undergo mitosis, and they were identified in light- and electron-microscopic preparations. The relationship between tetraploidy in the Purkinje cells during their postnatal differentiation and induction of mitosis in them by experimental means is discussed.

Perinatal development of conjugative enzyme systems.

The problems and priorities involved in studying the role of conjugagive enzymes in developmental pharmacology are discussed and evaluated. The relative rates of UDP glucuronyltransferase and beta-glucuronidase were studied during perinatal development in hepatic and extrahepatic tissues to determine the net balance of glucuronidation or deglucuronidation at different developmental stages. In general, deglucuronidation predominated over glucuronidation in fetal tissues whereas the converse was evident in adults. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an extremely toxic contaminant of some organochlorine compounds, was shown to be a potent inducer of some hepatic and extrahepatic drug-metabolizing enzymes. TCDD, administered during gestation, induced the postnatal activities of p-nitrophenol glucuronyltransferase and benzpyrene hydroxylase in rats. Foster mother experiments revealed that the postnatal induction was caused primarily by newborn exposure to TCDD in the mother's milk. Tissue distribution experiments with TCDD-14C confirmed these findings. Although TCDD induced non-steroid glucuronidation, no significant effects were evident on the postnatal development of steroid glucuronidation. The synthetic estrogen diethylstilbestrol (DES) is metabolized primarily by glucuronidation. The postnatal development of DES glucuronidation, like the steroid pathway, was not affected by gestational TCDD treatment. The fetal distribution of DES and DES-glucuronide, at different stages of development, correlated well with the perinatal development of steroid glucuronyltransferase activity.

The postnatal induction of threonine dehydratase in rat liver

1. 1. Administration of actinomycin D or cyclohcximide to rats at the time of surgical delivery results in complete repression of the development of threonine dehydratase activity. 2. 2. Precocious development of the enzyme may be brought about by injection of glucagon or adrenaline to foetal rats in utero. 3. 3. Dibutyryl-3′,5′-cyclic AMP potentiates the development of threonine dehydratase in the postnatal rat liver but is without effect on the induction of the enzyme in foetal liver.

Tyrosine α ketoglutarate transaminase in the liver of rats with intra-uterine growth retardation

The postnatal induction of TKT in the liver of rats submitted to intra-uterine growth retardation (I. U. G. R.) is much more greater than in the liver of normal animals. This striking rise in activity, seems to be related to the low blood glucose levels found in the I. U. G. R. animals. However glucagon injections to I. U. G. R. fetuses are not so efficient as in the case of the controls.

The postnatal induction of serine dehydratase in rat liver

1. 1. Postnatal development of serine dehydratase in rat liver in vivo is blocked by actinomycin D and cycloheximide. 2. 2. Glucagon induces enzyme activity in late foetal liver in utero and stimulates postnatal development twofold, as does tryptophan injection. 3. 3. Blockade of postnatal hypoglycaemia with glucose represses enyzme synthesis by 30 per cent but is without effect on the glucagon stimulation. 4. 4. Dibutyryl 3',5'-cyclic AMP stimulates postnatal synthesis of serine dehydratase nearly twofold; the effect is completely blocked by actinomycin D. 5. 5. Dibutyryl cyclic AMP and adrenaline do not induce enzyme activity in the rat foetus.

Multiple forms of soluble rat liver tyrosine aminotransferase premature induction and postnatal development

1. 1. The postnatal development of the multiple forms of tyrosine aminotransferase in rat liver shows that form C appears within 5 hours of birth, form B appears within 10 hours of birth, and form A appears about the third postnatal day. 2. 2. Injection of triamcinolone to rat foetuses in utero results in the appearance of form C of tyrosine aminotransferase within 24 hours followed by form B. 3. 3. Treatment of foetal animals in utero with glucagon leads to the appearance of form C of the enzyme within 5 hours while the same hormone treatment of 2-day postnatal rats leads to the appearance of both forms B and C. 4. 4. In surgically delivered rats adrenalcctomized within an hour of birth, the injection of glucagon in large doses is much less effective in promoting tyrosine aminotransferase synthesis than it is in unoperated litter-mate controls or in sham-operated animals. 5. 5. The role of glucagon, adrenal steroids, adrenaline, insulin, and cyclic AMP in the postnatal induction of hepatic tyrosine aminotransferase are all discussed in terms of the patterns of multiple enzyme development.