Oxygen toxicity causes all except
High-Yield Explanation
It is interesting that while O2 is necessary for life in aerobic organisms, it is also toxic. Indeed, 100% O2 has been demonstrated to exe toxic effects not only in animals but also in bacteria, fungi, cultured animal cells, and plants. The toxicity seems to be due to the production of reactive oxygen species including superoxide anion (O2 -) and H2O2. When 80-100% O2 is administered to humans for periods of 8 h or more, the respiratory passages become irritated, causing substernal distress, nasal congestion, sore throat, and coughing. Some infants treated with O2 for respiratory distress syndrome develop a chronic condition characterized by lung cysts and densities (bronchopulmonary dysplasia). This syndrome may be a manifestation of O2 toxicity. Another complication in these infants is retinopathy of prematurity (retrolental fibroplasia), the formation of opaque vascular tissue in the eyes, which can lead to serious visual defects. The retinal receptors mature from the center to the periphery of the retina, and they use considerable O2. This causes the retina to become vascularized in an orderly fashion. Oxygen treatment before maturation is complete provides the needed O2 to the photoreceptors, and consequently, the normal vascular pattern fails to develop. Evidence indicates that this condition can be prevented or ameliorated by treatment with vitamin E, which exes an antioxidant effect, and, in animals, by growth hormone inhibitors. Administration of 100% O2 at increased pressure accelerates the onset of O2 toxicity, with the production not only of tracheobronchial irritation but also of muscle twitching, ringing in the ears, dizziness, convulsions, and coma. The speed with which these symptoms develop is propoional to the pressure at which the O2 is administered; for example, at 4 atmospheres, symptoms develop in half the subjects in 30 min, whereas at 6 atmospheres, convulsions develop in a few minutes.Ref: Ganong review of medical physiology 23rd edition Page no: 622