CELL PROLIFERATIVE MODULATION OF MCG-101 SARCOMA FROM MICE EXPOSED TOHYPERBARIC OXYGENATION

Citation
E. Lyden et al., CELL PROLIFERATIVE MODULATION OF MCG-101 SARCOMA FROM MICE EXPOSED TOHYPERBARIC OXYGENATION, Undersea & hyperbaric medicine, 24(2), 1997, pp. 123-129
Citations number
44
Categorie Soggetti
Medicine, Research & Experimental","Marine & Freshwater Biology
ISSN journal
10662936
Volume
24
Issue
2
Year of publication
1997
Pages
123 - 129
Database
ISI
SICI code
1066-2936(1997)24:2<123:CPMOMS>2.0.ZU;2-D
Abstract
Tumor cell kinetics were studied in C57Bl/J mice with a transplantable sarcoma, MCG 101, exposed to hyperbaric oxygen (HBO2), 2.8 atm abs, 2 hours daily for 9 days or until spontaneous death. The isoenzymatic p attern of lactate dehydrogenase (LDH) confirmed that there was a signi ficant shift toward aerobic metabolism in tumor tissue as well as in t he liver and skeletal muscle. Recruitment of cells from the G(0)G(1) s tate into DNA synthesis was associated with an increased mobilization of substrates for polyamine synthesis in terms of an elevated ornithin e decarboxylase (ODC) activity. However, cell cycle turnover in terms of bivariate flow cytometric analysis after bromodeoxyuridine (BrdUrd) injection, final tumor weight, and survival time were not changed com pared with the controls. Tumor cell metabolism demonstrated evidence o f an unchanged net energy utilization, in that activities (V-max) of p hosphofructokinase (PFK) and LDH were not significantly changed. When the tumor-bearing animals were exposed to advanced HBO2 pressure (3.7 arm abs) for 3 h as a single dose, the DNA distribution and growth rat e were not changed immediately. However, 3.5 h later we observed a DNA pattern similar to that after repeated HBO2 treatments, 2.8 atm abs, concomitant with a preponderance of cells in the late S-phase, which i s consistent with a block at the entry of G(2)M. We conclude that MCG 101 sarcoma recovers from HBO2 exposure by an accumulation of cells in the S-phase without significant changes of net tumor growth. This may have relevance to clinical radiocurability.