Normoxia – Intracellular tissue normoxia is variable between organisms and tissues, and intracellular oxygen pressure is frequently well below air-level pO2 because of cellular (mainly mitochondrial) oxygen consumption and oxygen gradients along the respiratory cascade.
Hyperoxia is defined as environmental oxygen pressure above the normoxic reference level. Cellular and intracellular hyperoxia is imposed on isolated cells and isolated mitochondria at air-level oxygen pressures which are higher compared to cellular and intracellular oxygen pressures under tissue conditions in vivo.
Hypoxia is defined in respiratory physiology as the state when insufficient O2 is available for respiration, compared to environmental hypoxia defined as environmental oxygen pressures below the normoxic reference level. Three major categories of hypoxia are (1) environmental hypoxia, (2) physiological tissue hypoxia in hyperactivated states (e.g. at VO2max) with intracellular oxygen demand/supply balance at steady state in tissues at environmental normoxia, compared to tissue normoxia in physiologically balanced states, and (3) pathological tissue hypoxia including ischemia and stroke, anaemia, chronic heart disease, chronic obstructive pulmonary disease, severe COVID-19, and obstructive sleep apnea. Pathological hypoxia leads to tissue hypoxia and heterogenous intracellular anoxia.
Anoxia – Ideally the terms anoxia and anoxic (anox, without oxygen) should be restricted to conditions where molecular oxygen is strictly absent. Practically, effective anoxia is obtained when a further decrease of experimental oxygen levels does not elicit any physiological or biochemical response.
The experimentally applied O2 regime is an important factor in mitochondrial research. The Oxia enables quick and easy adjustment of the O2 concentration in the O2k chamber to cover a wide O2 range for experimental purposes.
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Oxia – the O2 regime controller for HyperOxia to HypOxia in the O2k
Gnaiger E (2003) Oxygen conformance of cellular respiration. A perspective of mitochondrial physiology. Adv Exp Med Biol 543:39-55. -»Bioblast link«