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The contribution made by cell death and oxygenation to 31 P MRS observations of tumour energy metabolism
Author(s) -
Tozer G. M.,
Griffiths J. R.
Publication year - 1992
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1940050515
Subject(s) - phosphocreatine , hypoxia (environmental) , glycolysis , oxygen , metabolism , oxidative phosphorylation , biology , programmed cell death , nucleoside triphosphate , oxygenation , cell , apoptosis , mitosis , cellular respiration , biochemistry , mitochondrion , energy metabolism , chemistry , microbiology and biotechnology , endocrinology , nucleotide , gene , ecology , organic chemistry
This review discusses the relationship between tumour oxygenation status, tumour cell death and the 31 P MRS parameters associated with cellular energy metabolism (phosphocreatine, nucleoside triphosphates and P 1 ). The presence of cells dying by apoptosis, and during mitosis would be unlikely to affect the 31 P spectrum directly since they represent only a small fraction of tumour cells and remain energized until phagocytosed. Histologically necrotic cells also probably contribute nothing to the 31 P spectrum. Instead, the spectrum appears to reflect the degree of hypoxia of the remaining viable cells, and the metabolic alterations required to sustain ATP synthesis as the oxygen supply diminishes. The biochemical theory developed to account for the 31 P spectra of acutely hypoxic tissues does not apply to chronically hypoxic tumours. The concentrations of free ADP and P 1 have major roles in the control of oxidative phosphorylation and glycolysis, as in normal tissues, but the precise relationships are still obscure. Cell‐killing following therapy may indirectly affect 31 P MRS parameters via changes in oxygen concentration brought about by an improvement in tumour blood flow and alterations in oxygen consumption rates and diffusion distances.