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Oxygen Toxicity: From Cough to Convulsion

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Part of the Oxidative Stress in Applied Basic Research and Clinical Practice book series (OXISTRESS)

Abstract

Oxygen is by its chemical nature a toxic molecule and organisms that survive in its presence have evolved potent antioxidant defenses. Through basic and clinical research we have come to understand many of the mechanisms of oxygen (O2) toxicity as well as measures that mitigate its risks. When the partial pressure of oxygen (PO2) is increased in the cell, the formation of reactive oxygen species (ROS) is enhanced at multiple locations, such as in the mitochondria. ROS attack biological macromolecules, which disrupts homeostasis and causes tissue and organ system dysfunction that will ultimately be lethal. An oxygen partial pressure (PO2) of 0.21 to 1.0 atm absolute (ATA) is in the normobaric range while a PO2 above 1.0 ATA is termed hyperbaric hyperoxia. As the PO2 in the normobaric range increases, specific physiological disturbances, such as disordered pulmonary gas exchange and retinopathy of prematurity appear, while others occur exclusively at hyperbaric pressures such as peripheral visual loss, seizures, and neurogenic pulmonary injury. Ultimately, the utility of O2 is limited by this toxicity and its therapeutic applications in medicine, aeronautics, and diving must be counterbalanced by the risk of harm.

Keywords

  • Hyperbaric
  • Normobaric
  • Hyperoxia
  • Oxygen toxicity
  • Hyperoxic myopia
  • Seizure
  • Nitric oxide
  • Neurogenic pulmonary edema

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Medford, M.A., Piantadosi, C.A. (2015). Oxygen Toxicity: From Cough to Convulsion. In: Roberts, S., Kehrer, J., Klotz, LO. (eds) Studies on Experimental Toxicology and Pharmacology. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Cham. https://doi.org/10.1007/978-3-319-19096-9_23

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