scholarly journals Ornithine decarboxylase induction in cells stimulated to proliferate differs from that in continuously dividing cells

1980 ◽  
Vol 188 (2) ◽  
pp. 375-380 ◽  
Author(s):  
Anne E. Cress ◽  
Eugene W. Gerner
Keyword(s):  
Enzyme Activity ◽  
Dna Synthesis ◽  
Ornithine Decarboxylase ◽  
Chinese Hamster Ovary Cells ◽  
Time Interval ◽  
Decarboxylase Activity ◽  
Quiescent Cells ◽  
Ornithine Decarboxylase Activity ◽  
Dividing Cells ◽  
In Cells

Ornithine decarboxylase activity increases at least 4–5-fold before DNA synthesis both in synchronous cycling cells and in quiescent cells stimulated to proliferate. The purpose of our experiments was to test whether the transient peaks of ornithine decarboxylase activity in both growth situations were biochemically regulated in a similar manner. We found that the regulation of this particular enzyme activity is distinct in two ways. Firstly, the addition of 2mm-hydroxyurea will block the induction of ornithine decarboxylase in continuously dividing Chinese-hamster ovary cells, while having no effect on ornithine decarboxylase induction in stimulated quiescent cells. Hydroxyurea added after the induction occurs has no effect on the enzyme activity. The apparent half-life of the enzyme is not altered in cells treated with hydroxyurea. Hydroxyurea does not affect the enzyme directly, since incubation of cell homogenates with this drug results in no loss of measurable ornithine decarboxylase activity and hydroxyurea does not markedly alter general RNA- or protein-synthesis rates. The inactivation of ornithine decarboxylase activity by hydroxyurea does not resemble the loss of activity observed with a 90min treatment with spermidine. Thiourea, a less potent inhibitor of ribonucleoside diphosphate reductase, will also inhibit ornithine decarboxylase activity, but to a lesser extent. Secondly, the expression of ornithine decarboxylase in quiescent cells stimulated to proliferate is biphasic as these cells traverse G1 and enter S phase, whereas only one peak of activity is apparent in synchronous cycling G1-phase cells. The time interval between the first peak of ornithine decarboxylase activity and the onset of DNA synthesis is approx. 5h longer in non-dividing cells stimulated to proliferate than in continuously dividing cells. The results suggest that the regulation of ornithine decarboxylase activity is different in the two growth systems in that the induction of ornithine decarboxylase in continuously dividing cells occurs closer in time to DNA synthesis and is dependent on deoxyribonucleoside triphosphates.

scholarly journals Ornithine decarboxylase activity and the onset of deoxyribonucleic acid synthesis in regenerating liver

1978 ◽  
Vol 170 (1) ◽  
pp. 123-127 ◽  
Author(s):  
J A McGowan ◽  
N Fausto
Keyword(s):  
Dna Synthesis ◽  
Ornithine Decarboxylase ◽  
Time Course ◽  
Deoxyribonucleic Acid ◽  
Acid Synthesis ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity ◽  
Low Protein ◽  
Deoxyribonucleic Acid Synthesis ◽  
Second Peak

Compared with normally fed animals, rats fed on a low-protein diet for 3 days exhibit a considerable delay in DNA synthesis after partial hepatectomy. In the regenerating livers of these animals (a) the timing of the first peak of ornithine decarboxylase activity is not altered and (b) the second peak of enzyme activity is delayed by a few hours, but polyamine concentrations are similar to those of normally fed rats. The results suggest that regardless of the possible effect of polyamines on DNA synthesis, the time course of ornithine decarboxylase activity appears to be independent of the onset of DNA replication in regenerating livers.

Ornithine decarboxylase activity and DNA synthesis in Morris hepatomas 51123-C and 7800

Life Sciences ◽  
1976 ◽  
Vol 18 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Michael W. Pariza ◽  
Susumu Yanagi ◽  
James A. Gurr ◽  
Donald E. Bushnell ◽  
Harold P. Morris ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Ornithine Decarboxylase ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity

Effects of Acute and Subchronic Exposure of Topically Applied Fullerene Extracts on the Mouse Skin

1993 ◽  
Vol 9 (4) ◽  
pp. 623-630 ◽  
Author(s):  
Mark A. Nelson ◽  
Frederick E. Domann ◽  
G. Tim Bowden ◽  
Stephen B. Hooser ◽  
Quintus Fernando ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Ornithine Decarboxylase ◽  
Mouse Skin ◽  
Tumor Formation ◽  
Skin Tumor ◽  
Toxic Effects ◽  
Exposure Level ◽  
Decarboxylase Activity ◽  
Ornithine Decarboxylase Activity ◽  
Acute Toxic

The recent discovery that fullerenes (C60) can be produced in macroscopic quantities has sparked much interest in the chemistry of this unusual molecule. Concerns have also arose about the potential carcinogenic effects of this molecule. We have addressed the potential acute and subchronic toxic effects of fullerenes applied in benzene on the mouse skin. The acute toxic effects measured in this study included epidermal DNA synthesis and the induction of ornithine decarboxylase activity in the epidermis. At the topical dose of fullerenes used in these studies (i.e., 200 ug), we found no effect on either DNA synthesis or ornithine decarboxylase activity over a 72 hour time course after treatment. The subchronic effects of the fullerenes as a mouse skin tumor promoter was assessed by repeatedly applying the chemical to the skin after initiation with the polycyclic aromatic hydrocarbon, 7,12-dimethlybenz-anthracene (DMBA). Repeated administration of the fullerenes for up to 24 weeks post-initiation did not result in either benign or malignant skin tumor formation, whereas promotion with the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the formation of benign skin tumors. Our data indicate that fullerenes applied in benzene at a likely industrial exposure level do not cause acute toxic effects on the mouse skin epidermis.

scholarly journals The effects of 24R,25-dihydroxycholecalciferol and of 1 α,25-dihydroxycholecalciferol on ornithine decarboxylase activity and on DNA synthesis in the epiphysis and diaphysis of rat bone and in the duodenum

1983 ◽  
Vol 214 (2) ◽  
pp. 293-298 ◽  
Author(s):  
D Sömjen ◽  
I Binderman ◽  
Y Weisman
Keyword(s):  
Vitamin D ◽  
Enzyme Activity ◽  
Ornithine Decarboxylase ◽  
Thymidine Incorporation ◽  
Single Injection ◽  
Fold Increase ◽  
Decarboxylase Activity ◽  
Long Bones ◽  
Vitamin D Metabolites ◽  
Ornithine Decarboxylase Activity

The effect of cholecalciferol metabolites on ornithine decarboxylase activity and on DNA synthesis in developing long bones was investigated in vitamin D-depleted rats. In the epiphysis there was a 6.4-fold increase in ornithine decarboxylase activity 5 h after a single injection of 24R,25-dihydroxycholecalciferol but not of 24S,25-dihydroxycholecalciferol or other vitamin D metabolites. In comparison, in the diaphysis and duodenum, 1 alpha,25-dihydroxycholecalciferol, but not other vitamin D metabolites, caused a 3-3.5-fold increase in the enzyme activity. The enzyme activity in the tissues examined attained a maximal value at 5 h after the injection of the metabolites. The activity of ornithine decarboxylase in the epiphysial region increased dose-dependently as the result of a single injection of 24R,25-dihydroxycholecalciferol and attained a maximal value at a dose between 30 and 3000 ng. In addition, administration of 24R,25-dihydroxycholecalciferol, but not 24S,25-dihydroxycholecalciferol or other metabolites, caused within 24 h a 1.7-2.0-fold increase in [3H]thymidine incorporation into DNA of the epiphyses of tibial bones. In comparison, 1 alpha,25-dihydroxycholecalciferol caused a 1.5-fold increase in [3H]thymidine incorporation into DNA of the diaphyses and of the duodenum. The present data indicate that 24R,25-dihydroxycholecalciferol is involved in the regulation of epiphyseal growth, whereas 1 alpha,25,dihydroxycholecalciferol stimulates the proliferation of cells in the diaphysis of long bones and in the intestinal mucosa.

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