ABSTRACT
The biochemical effects of hypoxia were studied in hepatocytes isolated from fasted rats. Protein synthesis is totally and immediately stopped when cells are incubated in hypoxia, while intracellular ATP content decreases progressively. The addition of fructose (a well- known glycolytic precursor) protects against hypoxic cell injury. Experimental data indicate that cells respond to oxygen limitation rather than to ATP depletion. We hypothesize that the rationale of such inhibition is to lead cells in a state of “metabolic arrest”, thus keeping ATP for more critical cellular functions. Such a hypothesis implies the existence of an “oxygen sensor” indicating to cells whether to stop or to reinitiate their biosynthetic activities.
