Role of Blood Flow vs. O2 Consumption in Nicotinamide-induced Increase pO2 in a Murine Tumor.
- Author:
Intae LEE
1
;
Moon June CHO
;
Thomas J DEMHARTNER
;
Leo E GERWECK
Author Information
1. Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
- Publication Type:Original Article
- Keywords:
Nicotinamide;
Oxygen consumption (QO2 );
Tumor blood flow (TBF);
Laser Doppler flowmetry
- MeSH:
Laser-Doppler Flowmetry;
Metabolism;
Niacinamide;
Oxygen;
Phosphates;
Tumor Burden
- From:Journal of the Korean Society for Therapeutic Radiology
1994;12(1):17-26
- CountryRepublic of Korea
- Language:English
-
Abstract:
We evaluated the effect of nicotinamide on cellular O2 consumption and metabolic status i.e., adenylate phosphates and NAD+ in-vitro, and changes in blood flow in-vivo, to determine whether changes in cellular metabolism or increased oxygen availability, was responsible for increased tumor oxygenation. Thirty min. Pre-incubation of cells with~4mM (=500mg/kg) nicotinamide resulted in no change in cellular O2 consumption. Similarly, neither the adenylate phosphates nor the cellular NAD+ levels were altered in the presence of~4mM nicotinamide. In-vivo, nicotinamide (500mg/kg) increased O2availability as estimated by changes in relative tumor blood flow (RBC flux). The changes in RBC flux measured by the laser Doppler method, were tumor volume dependent and increased from~35% in~150mmdegree tumors to~75% in~500mmdegree tumors. In conclusion, these observations indicate a reduction in local tissue O2 consumption is not a mechanism of improved tumor oxygenation by nicotinamide in FsaII murine tumor model. The primary mechanism of increased pO2 appears to be an increased local tumor blood flow.
