Low-dose radiation exposure induces a HIF-1-mediated adaptive and protective metabolic response.
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ABSTRACT: Because of insufficient understanding of the molecular effects of low levels of radiation exposure, there is a great uncertainty regarding its health risks. We report here that treatment of normal human cells with low-dose radiation induces a metabolic shift from oxidative phosphorylation to aerobic glycolysis resulting in increased radiation resistance. This metabolic change is highlighted by upregulation of genes encoding glucose transporters and enzymes of glycolysis and the oxidative pentose phosphate pathway, concomitant with downregulation of mitochondrial genes, with corresponding changes in metabolic flux through these pathways. Mechanistically, the metabolic reprogramming depends on HIF1α, which is induced specifically by low-dose irradiation linking the metabolic pathway with cel
SUBMITTER: Lall R
PROVIDER: S-EPMC3978308 | biostudies-literature | 2014 May
REPOSITORIES: biostudies-literature
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