The contribution made by cell death and oxygenation to31P MRS observations of tumour energy metabolism

摘要

AbstractThis review discusses the relationship between tumour oxygenation status, tumour cell death and the31P MRS parameters associated with cellular energy metabolism (phosphocreatine, nucleoside triphosphates and P1). The presence of cells dying by apoptosis, and during mitosis would be unlikely to affect the31P 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 the31P 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 the31P spectra of acutely hypoxic tissues does not apply to chronically hypoxic tumours. The concentrations of free ADP and P1have 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 affect31P MRS parameters via changes in oxygen concentration brought about by an improvement in tumour blood flow and alterations in oxygen consumption rates and diffusion distance