Effect of hypoxia on human seminoma cells

Fujii, Takaaki; Otsuki, Takemi; Moriya, Takuya; Sakaguchi, Haruko; Kurebayashi, Junichi; Yata, Kenichiro; Uno, Masako; Kobayashi, Tatsuya; Kimura, Tooru; Jo, Yoshimasa; Kinugawa, Keigo; Furukawa, Yoji; Morioka, Motohiro; Ueki, Ayako; Tanaka, Hiroyoshi

doi:10.3892/ijo.20.5.955

Cited by 20 publications

(19 citation statements)

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“…Adenine nucleotide degradation accompanied by a transient accumulation of Ado has been observed in ischemic rat tissue [8]. In cultured cells the rapid decrease of ATP levels following hypoxia is well known, although varying degrees of subsequent degradation of the nucleotides have been reported [53,54]. In the present experiments, ATP degradation during hypoxia appears to be dependent on cell density in HepG2 and HEK-293 cells.…”

Section: Discussionsupporting

confidence: 53%

S-Adenosylhomocysteine Metabolism in Different Cell Lines: Effect of Hypoxia and Cell Density

Hermes

Hippel²,

Oßwald³

et al. 2005

Cell Physiol Biochem

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Background/Aims: The methylation potential (MP) is defined as the ratio of S-adenosylmethionine (AdoMet) to S-adenosylhomocysteine (AdoHcy). It was shown recently that hypoxia increases AdoMet/AdoHcy ratio in HepG2 cells (Hermes et al., Exp Cell Res 294: 325-334, 2004). In the present study, we compared AdoMet/AdoHcy ratio and energy metabolism in HepG2, HEK-293, HeLa, MCF-7 and SK-HEP-1 cell lines under normoxia and hypoxia. Methods: Metabolite concentrations were measured by HPLC. In addition, AdoHcy hydrolase (AdoHcyase) activity was determined photometrically. Results: Under normoxia HepG2 cells show the highest AdoMet/AdoHcy ratio of 53.4 ± 3.3 followed by MCF-7 and SK-HEP-1 cells with a AdoMet/AdoHcy ratio of 14.4 ± 1.1 and 21.1 ± 1.3, respectively. The lowest AdoMet/AdoHcy ratios are exhibited by HeLa and HEK-293 cells (6.6 ± 0.7 and 7.1 ± 0.3). Hypoxia does not significantly change the MP in MCF-7 and HeLa cells, but alters the MP in HepG2, HEK-293 and SK-HEP-1 cells. These alterations are dependent on the cell density. Under normoxia HepG2 cells exhibit AdoHcyase activity of 2.5 ± 0.2 nmol min^-1 mg^-1 protein. All other cell lines show 3-5 times lower enzyme activity. Interestingly, hypoxia affects AdoHcyase activity only in HepG2 cells. Conclusions: Our data clearly show that the cell lines are characterized by different MP and different behavior under hypoxia. That implies that a lower MP is not necessarily associated with impaired transmethylation activity and cellular function.

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Section: Discussionsupporting

confidence: 53%

S-Adenosylhomocysteine Metabolism in Different Cell Lines: Effect of Hypoxia and Cell Density

Hermes

Hippel²,

Oßwald³

et al. 2005

Cell Physiol Biochem

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“…This reduction in cell proliferation was not seen in anaemic animals using the same tumour model , presumably because anaemia resulted in an increase of tumour hypoxia, which is less pronounced than that seen when animals were subjected to an atmosphere containing only 8% oxygen. Even though the proliferation rate was reduced in the present study, a cell cycle arrest in the G 1 phase, as has been described in cell culture experiments (Fujii et al, 2002), was not found in the in vivo situation in the present study. The fraction of cells in the G 0 /G 1 phase in tumours under hypoxic conditions was not significantly increased as compared to controls breathing room air.…”

Section: Discussioncontrasting

confidence: 41%

Microenvironmental adaptation of experimental tumours to chronic vs acute hypoxia

et al. 2004

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This study investigated long-term microenvironmental responses (oxygenation, perfusion, metabolic status, proliferation, vascular endothelial growth factor (VEGF) expression and vascularisation) to chronic hypoxia in experimental tumours. Experiments were performed using s.c.-implanted DS-sarcomas in rats. In order to induce more pronounced tumour hypoxia, one group of animals was housed in a hypoxic atmosphere (8% O 2 ) for the whole period of tumour growth (chronic hypoxia). A second group was acutely exposed to inspiratory hypoxia for only 20 min prior to the measurements (acute hypoxia), whereas animals housed under normal atmospheric conditions served as controls. Acute hypoxia reduced the median oxygen partial pressure (pO 2 ) dramatically (1 vs 10 mmHg in controls), whereas in chronically hypoxic tumours the pO 2 was significantly improved (median pO 2 ¼ 4 mmHg), however not reaching the control level. These findings reflect the changes in tumour perfusion where acutely hypoxic tumours show a dramatic reduction of perfused tumour vessels (maybe the result of a simultaneous reduction in arterial blood pressure). In animals under chronic inspiratory hypoxia, the number of perfused vessels increased (compared to acute hypoxia), although the perfusion pattern found in control tumours was not reached. In the chronically hypoxic animals, tumour cell proliferation and tumour growth were significantly reduced, whereas no differences in VEGF expression and vascular density between these groups were observed. These results suggest that long-term adaptation of tumours to chronic hypoxia in vivo, while not affecting vascularity, does influence the functional status of the microvessels in favour of a more homogeneous perfusion.

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“…However, this may be a unique characteristic of non-seminoma cells, such as EC, since seminoma cells cultured at low oxygen concentrations enter the G 1 cell cycle arrest phase. 74 Neoplastic stem cells located in hypoxic areas may also produce vascularization-promoting factors that activate the angiogenic switch. However, in such a microenvironment, with uncontrolled cell growth and disturbed growth factor gradients, the newly constituted vessels are poorly formed, tortuous and leaky, and do not fulfill their oxygen-transportation function.…”

Section: Conclusion and Prospectivesmentioning

confidence: 99%