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At least 559 records · Page 31Linked to original sources
PubMed1999

Activation of the adult mode of ovine growth hormone receptor gene expression by cortisol during late fetal development.

The developmental and tissue-specific regulation of growth hormone receptor (GHR) mRNA expression is complex and involves alternate leader exon usage. The transcript composition of hepatic GHR mRNA has therefore been determined in fetal sheep during late gestation and after experimental manipulation of fetal plasma cortisol levels by fetal adrenalectomy and exogenous cortisol infusion, using RNase protection assays and a riboprobe containing exons 1A, 2, and 3 of the ovine GHR gene. Expression of the adult liver-specific GHR mRNA transcript containing exon 1A was not detected earlier than 138 days of gestation (term 145 +/-2 days). Thereafter, expression of this leader exon increased and accounted for 25-30% of the total GHR mRNA in the fetal liver at term. Hepatic GHR mRNA derived from leader exons other than 1A was detectable at 97 days and increased in abundance toward term in parallel with the normal prepartum rise in fetal plasma cortisol. Abolition of this cortisol surge by fetal adrenalectomy prevented both the activation of exon 1A expression and the prepartum rise in GHR mRNA derived from the other leader exons in fetal ovine liver. Conversely, raising cortisol levels by exogenous infusion earlier in gestation prematurely activated exon 1A expression and enhanced the abundance of GHR mRNA transcripts derived from the other leader exons. Cortisol therefore appears to activate the adult mode of GHR gene expression in fetal ovine liver during late gestation. These observations have important implications for the maturation of the somatotrophic axis and for the onset of GH-dependent growth after birth.

Adrenalectomy↗
PubMed2004

Role of redox in fetal development and neonatal diseases.

In the cell, reducing and oxidizing molecules modulate the redox state. In embryonic and fetal growth, increased oxidative stress may be detrimental, but an oxidized state can also be beneficial. This is because redox may also affect key transcription factors that can alter gene expression during development. In addition, redox may impact on placentation and amniotic membrane integrity during pregnancy. Lastly, diseases of prematurity, such as necrotizing enterocolitis, retinopathy of prematurity, and chronic lung disease, may be modulated by redox in the premature. Because antioxidant therapies have not necessarily modified the outcome of these diseases, some debate exists as to this. Nonetheless, sufficient evidence suggests a role for redox throughout embryonic, fetal, and postnatal development. This evidence will be explored here.

Animals↗
PubMed1987

Effects of caffeine administered during pregnancy on fetal development and subsequent function in the adult rat: prolonged effects on a second generation.

Caffeine, when administered in moderate (30 mg/kg X d) or high (60 mg/kg X d) doses during pregnancy, was shown to cause significant fetal growth retardation of both sexes. Mortality rate at or soon after birth was significantly higher and litter size significantly lower in the litters treated with 60 mg. The subsequent growth rates were also affected. The experimental pups grew more slowly, with growth plateauing at the same age resulting in smaller adults. The male offspring when subjected to short-term stress (one session) in adulthood showed an intact emergency response, demonstrating an adequate ability to react to a sudden environmental change. A significant decrease in 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity, and consequent reduction in testosterone biosynthesis, in the fetal testes at d 18 and 20 of gestation was also found for both doses of caffeine. Low 3 beta-HSD activity persisted to adulthood in the group receiving 60 mg. Lingering effects were observed in a second litter bred 8 wk after the discontinuation of caffeine consumption. In this second breeding, the offspring of both sexes from both caffeine doses were born significantly smaller when compared to the controls. Persistent effects of caffeine were also found in second-generation rats bred from females who were exposed to caffeine in utero. The pups of both sexes were born significantly heavier after a significantly longer gestation. The subsequent growth did not differ from that of the controls. It was suggested that a changed genetic program in the ovarian germ cells of the first generation and/or a changed uterine environment in the second generation may be implicated.

3-Hydroxysteroid Dehydrogenases↗
PubMed1990

Xanthine oxidase during human fetal development.

Through oxygen free-radical production, xanthine oxidase (XOD, E.C.1.2.3.2) has been implicated in the pathogenesis of postischemic and hyperoxic tissue injuries among newborn. We measured the activity and evaluated the kinetic characteristics of XOD in human fetal liver, intestine, brain, and myocardium. Both the fetal liver and intestine contain a high XOD activity through gestation. The activity increases in the liver and decreases in the intestine with advancing gestation. The apparent Km for hypoxanthine is 4.8-5.5 microM in the intestine throughout gestation and in the liver at term but higher than 30 microM in the liver during the first half of pregnancy. The activity is undetectable both in the fetal brain and myocardium throughout gestation. Thus, XOD activity is present at least in the liver and intestine to account for the oxidation of hypoxanthine and xanthine. However, direct evidence for adenine nucleotide catabolism, followed by oxidation of the accumulated hypoxanthine during tissue reoxygenation in the human liver or intestine is not available.

Brain↗
PubMed1976

Expression of an oncodevelopmental gene product (alpha-fetoprotein) during fetal development and adult oncogenesis.

The expression of an "oncodevelopmental" protein, alpha-fetoprotein (AFP), has been systematically studied in rats during normal development and during regeneration of the liver by fetal rat hepatocytes in vitro, in rats bearing transplantable hepatomas, in rats fed chemical carcinogens, and in mice that spontaneously develop hematomas. AFP is a serum protein made normally during fetal and neonatal stages by liver and yolk sac cells. In newborn rats at approximately 4 weeks of age, the production of AFP is abruptly terminated, a process which is closely associated with cessation of liver cell proliferation. In adult rats, AFP production recurs following the reinitiation of hepatic DNA synthesis induced by partial hepatectomy or by the administration of heaptotoxic chemicals. Detailed metabolic and direct labeling studies of fetal rat hepatocytes in vitro also demonstrate a kinetically similar pattern of hepatocyte DNA synthesis and AFP production. In vitro studies utilizing combined autoradiography for DNA-synthesizing cells and immunofluorescence for AFP-containing cells demonstrates that replicating hepatocytes produce AFP, however, available data do not yet permit a distinction between G1 (pre- or postmitotic) and/or G2 production. During growth of an AFP- producing tumor, the serum concentration of AFP may be used as a accurate index of tumor growth, and, if a transplanted tumor is removed, as a marker for metastatic growth of the tumor. Using this model, we have shown that radiation to the lung at the time of surgical removal of a growing tumor in the leg will prevent establishment and growth of pulmonary metastases and that anti-AFP serum treatment may inhibit growth of a transplantable hepatoma that produces AFP. The exposure of rats to chemical hepatocarcinogens results in the appearance of evaluated serum AFP concentration as early as within 1 week of feeding; noncarcinogenic chemical analogs do not cause an elevation. AFP elevation also occurs with low doses of the hepatocarcinogen in the absence of detectable cell injury (by morphological examination of serum enzyme levels) or any other known morphological or biochemical change. This may represent a highly selective derepression of protein synthesis that occurs following the formation of a complex between the metabolites of the carcinogen and specific chromatin loci. Although every rat so far treated with even subcarcinogenic doses of hepatocarcinogens has elevated serum AFP concentrations, many primary carcinogen-induced hepatomas do not produce detectable AFP. Either there is a subsequent change in the preneoplastic AFP-producing cell that occurs prior to irreversible neoplastic alteration, or the hepatocytes originally influenced by the carcinogens to produce AFP are not necessarily the same cells that are the progenitors of the hepatoma produced by more prolonged exposure...

2-Acetylaminofluorene↗
PubMed2003

Effect of trihalomethane exposure on fetal development.

AIMS: To examine the effect of trimester specific and pregnancy average total trihalomethane (TTHM) exposure on infant birth weight, low birth weight, and intrauterine growth retardation in term births, as well as gestational age and preterm delivery in all births. METHODS: Cross sectional analysis of 56 513 singleton infants born to residents of Massachusetts during 1990. City specific aggregate data were used to estimate maternal exposure to TTHM concentration; individual maternal information was used to adjust for confounding. RESULTS: Increased pregnancy average and second trimester TTHM exposure were associated with small for gestational age and reductions in birth weight after adjusting for potential confounding variables. Compared to </=60 micro g/l, pregnancy average TTHM exposure over 80 micro g/l was associated with a 32 g reduction in birth weight. There was a 23 g reduction in birth weight in infants born to mothers exposed to greater than 80 micro g/l TTHM during the second trimester. For each 20 micro g/l increase in TTHM, the estimated reduction in birth was 2.8 g for pregnancy average exposure and 2.6 g for second trimester exposure. An increased risk of small for gestational age births was found for pregnancy average (odds ratio (OR) 1.14; 95% CI 1.02 to 1.26) and second trimester (OR 1.13, 95% CI 1.03 to 1.24) TTHM levels greater than 80 micro g/l. There was no evidence of an association between preterm delivery and increased TTHM levels, but there were slight increases in gestational duration associated with TTHM concentrations. CONCLUSIONS: Maternal exposure to THMs may be associated with fetal growth retardation. Our findings are consistent with most previous work, although we generally found smaller effects of TTHMs on low birth weight and intrauterine growth retardation.

Adolescent↗