Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of postnatal methyl mercury exposure on the ontogeny of renal and hepatic responsiveness to trophic stimuli were examined. Increased ornithine decarboxylase (ODC) activity was used as an index of tissue stimulation. In the rat, renal ODC responsiveness to growth hormone, angiotensin, vasopressin, isoproterenol, and serotonin was absent at birth and matured 3 to 4 weeks later. However, pups exposed to methyl mercury showed marked, ODC responses to these same agents as early as 10 to 19 days of postnatal age, accompanied by a significant renal hypertrophy. In contrast to the kidney, the liver of normally developing rats was responsive to trophic factors even in the neonate. In this tissue, there was no consistent effect of neonatal methyl mercury treatment on ODC responses at any developmental stage tested; although absolute liver weights were reduced, liver/body weight ratio was not affected. These results demonstrate that postnatal methyl mercury exposure causes a precocious onset of ODC responses to trophic agents specifically in the kidney. Altered responsiveness may mediate some of the effects of this organomercurial on overall renal development and function.
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PMID:Postnatal methyl mercury exposure: effects on ontogeny of renal and hepatic ornithine decarboxylase responses to trophic stimuli. 402 2

To determine the organ specificity of neonatal mercury hydroxide (CH3HgOH) exposure on biochemical development of its potential target tissues, effects on rat brain, liver, heart and kidney were compared utilizing the ontogenetic pattern of ornithine decarboxylase (ODC) activity, an early index of perturbation of cellular maturation. CH3HgOH was given daily beginning at birth for up to 21 days, using three dose levels (1, 2.5 or 5 mg/kg s.c.). In the brain, CH3HgOH treatment resulted in an initial reduction in ODC followed by a subsequent elevation of activity, a maturational pattern known to be associated with delayed cellular development. In contrast to the effects of CH3HgOH on brain, the pattern obtained in the liver, an initial elevation followed by a subsequent decline, is usually associated with compression of the time couse of cellular development. In the heart and kidney, CH3HgOH produced sustained elevations of ODC representing prolongation of the developmental period of rapid tissue growth and development; these patterns were associated with tissue hypertrophy which was sustained through the preweaning stage for both tissues and well into the postweaning period for the kidney. The results obtained with ODC clearly demonstrate that neonatal CH3HgOH poisoning causes organ-specific biochemical lesions which can play a role in subsequent effects on overall tissue development.
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PMID:Organ specificity of neonatal methyl mercury hydroxide poisoning in the rat: effects of ornithine decarboxylase activity in developing tissues. 714 71

The thymus of young rats contained a high basal activity of ornithine decarboxylase (ODC). Treatment with zinc sulphate caused a slight increase of thymic ODC activity within 6 hours and a more marked enhancement (three-fold) in the spleen 24 h after treatment. In spite of the high activity of thymic ODCin vivo, ODC was not detectable in primary cultures of rat thymocytes, but was early and largely induced after treatment with Concanavalin A (Con A). The presence of 0.1 mM zinc in the medium increased the response of ODC to Con A. This effect of zinc in mitogen activated thymocytes may be due to the stabilization of ODC, which was found to decay with a half life of 65 min after the block of protein synthesis with cycloheximide. On the contrary in absence of zinc the half life of the enzyme was 40 min, as in the rat thymus in vivo.Zinc alone, at 0.1 mM concentration, did not affect ODC activity in resting thymocytes during the early times, but the metal was able to cause an increase of the enzyme activity after 4-6 days of culture. Other heavy metals such as mercury, cadmium and copper provoked a late increase of ODC activity, but their action was evident only at dosages which were toxic for the cells.
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PMID:Zinc can influence ornithine decarboxylase activity in rat thymus cells. 2419 May 57