Citronellal suppress the activity of ornithine decarboxylase in hypopharyngeal carcinoma cells

Author(s):  
Kaneez Fatima ◽  
Suaib Luqman
1982 ◽  
Vol 202 (1) ◽  
pp. 267-270 ◽  
Author(s):  
L Alhonen-Hongisto ◽  
P Veijalainen ◽  
C Ek-Kommonen ◽  
J Jänne

Three out of four different mycoplasma strains analysed for the polyamine contents contained relatively high concentrations of putrescine, cadaverine, spermidine and spermine. In addition to ornithine decarboxylase (EC 4.1.1.17) activity, the mycoplasmas also exhibited comparable or higher lysine decarboxylase (EC 4.1.1.18) activity fully resistant to the action of 2-difluoromethylornithine, an irreversible inhibitor of eukaryotic ornithine decarboxylase. 2-Difluoromethylornithine did not modify the polyamine pattern of actively growing mycoplasmas. Ehrlich ascites carcinoma cells and L1210 mouse leukemia cells infected with any of the four mycoplasma strains contained, in addition to putrescine, spermidine and spermine, and also easily measurable concentrations of cadaverine; the latter diamine was absent in uninfected cultures. When the infected cells were exposed to difluoromethylornithine, the accumulation of cadaverine was markedly enhanced. The modification of cellular polyamine pattern by mycoplasmas, especially in the presence of inhibitors of eukaryotic ornithine decarboxylase, could conceivably be used as an indicator of mycoplasma infection in cultured animal cells.


1985 ◽  
Vol 229 (3) ◽  
pp. 711-715 ◽  
Author(s):  
L Alhonen-Hongisto ◽  
A Kallio ◽  
R Sinervirta ◽  
O A Jänne ◽  
C G Gahmberg ◽  
...  

We selected a 2-difluoromethylornithine-resistant Ehrlich ascites-carcinoma cell line that grows in the presence of 20 mM-difluoromethylornithine. These cells contain 10-20 times the normal amount of hybridizable sequences for ornithine decarboxylase (EC 4.1.1.17) in their genomic DNA. We used these gene-amplified cells, their revertant counterparts (grown in the absence of the drug after an established gene amplification) and tumour cells grown in the presence of putrescine to investigate the changes of ornithine decarboxylase gene pattern and simultaneously occurring phenotypic changes, such as tumourigenicity and the expression of cell-surface glycoproteins. In the tumour cells reverted back to the normal gene frequency, not only did the amplified sequences disappear, but there were also signs of gene re-arrangements seen as a ‘gene jump’, when a signal evidently moved to a heavier restriction fragment. Similar gene re-arrangement likewise occurred in cells exposed to putrescine. Although the wild-type tumour cells and the gene-amplified cells readily grew in the peritoneal cavity of mice, the revertant cells and the putrescine-treated cells had lost their tumourigenicity in mice. Gene-amplified tumour cells and the revertant cells showed distinct changes in their surface glycoprotein pattern in comparison with the parental cell line. These findings indicate that alterations of ornithine decarboxylase gene pattern/dosage may be associated with phenotypic changes possibly related to the tumourigenicity of these carcinoma cells.


1992 ◽  
Vol 20 (10) ◽  
pp. 2581-2590 ◽  
Author(s):  
Jeffrey A. Moshier ◽  
David L. Osborne ◽  
Magdalena Skunca ◽  
Julie Dosescu ◽  
Jeffrey D. Gilbert ◽  
...  

2012 ◽  
Vol 4 (1) ◽  
pp. 7 ◽  
Author(s):  
Jia-Jun Tian ◽  
Su-Mei Lu ◽  
Liang Yu ◽  
Ju-Ke Ma ◽  
Ya-Kui Mu ◽  
...  

1985 ◽  
Vol 126 (2) ◽  
pp. 734-740 ◽  
Author(s):  
L. Alhonen-Hongisto ◽  
A. Kallio ◽  
R. Sinervirta ◽  
P/ Seppänen ◽  
K.K. Kontula ◽  
...  

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