Lung hypoxia is related, in acute form, to the increase of the pulmonary artery pressure, epithelial malfunction, edema, and lung inflammation. Thus, this condition is also a factor in various lung pathological processes like in obstructive sleep apnea (OSA), acute lung injury, asthma attacks, atelectasis, chronic obstructive pulmonary disease, and idiopathic pulmonary hypertension. The generation of hypoxia occurs when staying at high-altitude environments or when receiving mixtures of contaminated gases. This is especially significant in the light of the known toxic effect of this gas, although there are precedents of lung malfunction under low oxygen pressure conditions or hypoxia. Lung's main function is the exchange of gases, hence, it is the organ which makes contact with the higher pressure of oxygen in our body. Herein, studies of cultures of different lung cells and complete isolated lung and tests conducted in vivo in the different forms of hypoxia, conducted in both animal models and humans, are described. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed.
Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. This organ can be affected by hypoxia facing both physiological and pathological situations. One of the most important functions of lungs is to maintain an adequate oxygenation in the organism.
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