For each mole of glucose metabolised, anaerobic respiration (glycolysis) generates only 2 ATP moles compared to approximately 28–30 from oxidative phosphorylation. O 2 is the terminal electron acceptor at Complex IV of the electron transport chain (ETC), being reduced to water in this process. Over 90% of O 2 consumption is utilised by mitochondria, predominantly for ATP production (oxidative phosphorylation), but also for heat generation through uncoupling, and superoxide production. superoxide, peroxide, and hydroxyl anion). ROS are even more reactive molecules formed through oxygen’s electron receptivity (e.g. O 2 performs its actions through these unpaired electrons which act as radicals. Oxygen generally exists as di-atomic molecule (O 2) its two atoms bond to each other through single bonds leaving two unpaired electrons. The most important clinical studies are listed in Table 1 “Additional file 1” shows the complete study list. Figure 1 summarises the possible dangers of hyperoxia, highlighting pathophysiological mechanisms and their impact on specific disease conditions. This review discusses potential harms of O 2 in various underlying critical illnesses. Consequently, O 2 toxicity, especially pulmonary, is a matter of concern, and optimal dosing remains unclear in critical care. ROS are as “Janus-headed” as O 2: ROS are vital for host defence, and also toxic. This is particularly pronounced during ischaemia/reperfusion (I/R) and/or hypoxia/re-oxygenation. inspiratory O 2 concentrations (F IO 2) > 0.21, may cause hyperoxaemia (arterial PO 2 > 100 mmHg) and subsequently increased ROS formation. It is vital for aerobic respiration within the mitochondria, yet mitochondrial respiration also forms reactive oxygen species (ROS), production of which relates to O 2 concentration. Since its discovery, oxygen (O 2) has been recognised as “friend and foe”.
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