Hyperoxia in Intensive Care and Emergency Medicine: Dr. Jekyll or Mr. Hyde? An Update

Since the discovery of molecular oxygen (O2) at the end of the 18th century, its ‘friend and foe’ character has been recognized. On the one hand, O2 is vital for survival of mammalian cells since it allows for a sustained, high synthesis rate of adenosine triphosphate (ATP) in the respiratory chain because of its unique properties as a final electron acceptor [1]. On the other hand, this chemical property also renders it one of the strongest oxidizing agents that can damage any biological molecule [1], a phenomenon which led to the paradigm of ‘oxygen toxicity’. Oxygen toxicity is the result of enhanced formation of reactive oxygen species (ROS), the rate of formation being directly related to the O2 partial pressure [2]. The ambiguous role of O2 as a crucial molecule for ATP synthesis in the respiratory chain is also valid in the context of ROS formation. Approximately 1–3% of mitochondrial O2 consumption leads to ROS production; in other words, the more ATP is produced, the more ROS are released [2]! Moreover, ROS share the Janus-headed character of O2: While their toxic potential is well-established, they are also vital, both for host defense and as signaling molecules [3].