Oxygen metabolism and neutrophil function

It has been known for many years that the oxygen metabolism of neutrophils is unusual. As long ago as 1933 Baldridge and Gerard recognised the importance of oxygen for bacterial killing when they observed a ‘respiratory burst’ of increased O2 uptake that accompanied phagocytosis. It was known that, in most cells, O2 was needed to generate energy during mitochondrial respiration, and hence the respiratory burst was mistakenly thought to be required to supply the extra energy needed for the physical processes involved in phagocytosis. It was not until 1959 that the unusual nature, and hence the unusual enzyme system, of the respiratory burst was revealed, when it was shown that phagocytosis and bacterial killing could occur in neutrophils where mitochondrial respiration was poisoned by cyanide. This discovery led to the conclusion that the respiratory-burst enzyme has nothing to do with mitochondrial respiration, and so the extra O2 consumed must serve some other purpose in phagocytosing neutrophils. In fact, mature neutrophils possess very few, if any, active mitochondria, and they obtain their ATP for energy-utilising processes from glycolysis, a process thst does not require O2 supply. This independence of energy generation on O2 supply is important because it means that many neutrophil functions can occur efficiently in the O2-depleted environments that may be found in certain pathological circumstances (e.g. in inflamed tissues). Yet if O2 was not needed by phagocytosing neutrophils for oxidative phosphorylation, then for what other purpose was it required?