Manual Biological Oxidants: Generation and Injurious Consequences. Volume 4

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Lung injury is demonstrated to be caused directly by ROS production in response to hyperoxia and indirectly by ROS due to phagocyte activation and inflammation. The two mechanisms seem to be integrated In vitro and in vivo exposures to hyperoxia result in downregulation of peroxisome proliferators-activated receptor gamma and in increase transdifferentiation of pulmonary protective lipofibroblasts to myofibroblasts MYFs 50 , Epithelial cell growth and differentiation is not adequately supported by MYFs.

This results in a disturbed alveolarization, characterizing bronchopulmonary dysplasia BPD High level of neutrophils, IL-8, and leukotrienes in alveolar fluid of BPD infants clearly support the role of inflammation and ROS in the development of this oxidative damage The exposure to hyperoxia is also associated with higher risk for severe retinopathy of prematurity ROP , due to susceptibility of the phospholipid-rich retina to ROS The peripheral temporal portion of the retina is the last to be vascularized, and it is still immature even at term These mechanisms finally lead to abnormal retinal vascular proliferation and the formation of a ridge, which places traction on the retina and increases the risk of detachment, as seen in ROP Newborn erythrocytes are more prone to damaging effects of oxidative stress and to have higher content of free iron than those of adults.

In this context, free radical damage is involved in neonatal hemolytic anemia and particularly of the preterm 58 , Furthermore, prolonged exposure to hyperbaric oxygen leads to changes of erythrocytes shape, as a consequence of toxic effects of oxygen on the erythrocyte membranes.

In an animal model, various forms of abnormal red blood cells are observed after exposure to high oxygen concentration, and in particular echinocyte shape was dominated Exposure to hyperoxia at birth can also be related to long-term pathological effects. Furthermore, the exposure of newborn mice to hyperoxia may lead to long-term cardiac abnormalities, such as left ventricular dysfunctions 63 , and neurodevelopmental impairments in adult life, as demonstrated by abnormal behavior, deficits in spatial and recognition memory, small hippocampal dimensions, in the absence of intracranial pathology such as intraventricular hemorrhage or periventricular leukomalacia in the neonatal period In conclusion, experimental studies and clinical observations demonstrated high susceptibility of the fetus and newborn to oxidative stress.

Increased release and decreased detoxification in the newborn appear to be negatively correlated with the gestational age. Avoidance of conditions, such as infections, asphyxia, retinal light exposure, iron supplementation, and, in particular, hyperoxia, reduces oxidative stress. Recent studies, that have been accomplished, have revised the concept of the optimal oxygenation in newborns, children, and adults.

Chow et al. They found a decrease of incidence of ROP in the group treated with lower O 2 saturation without any differences in mortality and morbidity Neonatal outcomes showed that newborns treated with higher level of oxygen had more cognitive disabilities than those treated with lower oxygen, after 10 years But, as secondary outcome, they showed an increased incidence of chronic lung disease and a longer duration of hospitalization, both in the higher group.

Thanks to these data, it was possible to conduct a prospective meta-analysis, NeOProM 73 study, with a primary outcome defined as a composite of death and disability at 18—24 months of corrected age. The study showed no significant differences in the primary outcome, but the use of a lower range of oxygen saturation results in a decrease of occurrence of severe ROP and an increase of death before the discharge. The COT study, with a primary outcome defined as death before 18 months of corrected age or survival with one or more disability, do not showed significant differences in the mortality or other outcome, but only a reduction of duration of O 2 therapy.

However, there are more unanswered questions and the optimal oxygen saturation range for low birth weight preterm infants remains elusive. This is mainly due to the several different clinical conditions of preterm newborns. Some authors indicate that 50 and 70 mmHg 75 is the optimal oxygen tension, but it is noteworthy that pulse oximetry ability remains controversial. In clinical practice, the continuous monitoring of oxygen saturation is mandatory to titrate oxygen therapy as better as possible and the routine use of pulse oximetry systems can be considered a very useful approach for the neonatologists, in order to reach this goal.

However, the optimal target range for oxygen saturation in the sick newborns and, above all, in the extremely preterm babies is not clear. The challenge for the clinicians is reaching a balance in the oxygen administration, to avoid the damage and negative outcomes, associated with either hyperoxemia or hypoxemia.

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Based on all the actually available evidence and considering the lack of evidence about the influence of many factors such as transfusional status, different gestational ages and underlying diseases, the most careful approach is to avoid both hypoxia and hyperoxia in infants requiring oxygen supplementation.

It is essential to control the low limit as well as the upper limit to prevent excessive fluctuations of oxygen saturation 78 , Hyperoxia and hypoxia are deeply involved in the development of several neonatal diseases, and the mechanisms are complex and not yet fully understood. However, evidences suggest that both the generation of oxidant species i.

Hyperoxia and inflammation as well as the episode of hypoxia—reoxygenation and free iron appear to be sources of increased ROS release, which may cause tissue injury either by direct effect or as consequences of endothelium dysfunction and gene alteration, particularly in preterm newborns. Understanding the effects of O 2 administration is important for the management of oxygen therapy in newborns, in order to prevent inadvertent cellular and tissue damage caused by hyperoxia, in the patients requiring supplemental oxygenation.

SP: wrote a draft and supervised the final manuscript; CB: assisted with preparation of manuscript; NV: assisted with preparation of manuscript; GB: conceived the idea and supervised the final manuscript. The authors declare that there is no commercial or financial relationship that could be constructed as a potential conflict of interest.

Consequences of hyperoxia and the toxicity of oxygen in the lung. Nurs Res Pract Smith JL. The pathological effects due to increase of oxygen tension in the air breathed. J Physiol 24 1 — Studies on the effect of high oxygen administration in retrolental fibroplasia.


  • American Survival Guide (September/October 2015).
  • Symptoms of oxidative stress.
  • Advances in School Effectiveness Research and Practice.

Nursery observation. Am J Ophthalmol 35 9 — Halliwell B. Reactive oxygen species in living systems: source, biochemistry, and role in human disease. Active Oxygen in Chemistry , Vol. Google Scholar. Redox interplay between mitochondria ad peroxisomes. Front Cell Dev Biol — Holmstrom KM, Finkel T. Cellular mechanisms and physiological consequences of redox-dependent signals. Nat Rev Mol Cell Biol 15 6 — Reactive oxygen species as double-edged swords in cellular processes: low-dose cell signaling versus high-dose toxicity.

Hum Exp Toxicol —5. Buonocore G, Groenendaal F. Anti-oxidant strategies. Semin Fetal Neonatal Med — Reactive oxygen species and compartmentalization. Front Physiol Vento M. Oxygen supplementation in the neonatal period: changing the paradigm. Neonatology 4 — Novel sources of reactive oxygen species in the human body. Nephrol Dial Transplant 22 5 —8. Exposure to supplemental oxygen downregulates antioxidant enzymes and increases pulmonary arterial contractility in premature lambs. Neonatology — Exposure to supplemental oxygen and its effects on oxidative stress and antioxidant enzyme activity in term newborn lambs.

Pediatr Res — Prenatal development of lung antioxidant enzymes in four species. J Pediatr — Evidence of oxidative stress in full-term healthy infants.

Chlorine dioxide as a disinfectant

Expression and development profile of antioxidant enzymes in human lung and liver. Studies of tocopherol deficiency in infants and children. Hemolysis of erythrocytes in hydrogen peroxide. Am J Dis Child — Am J Clin Nutr —9.

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Expression and developmental profile of antioxidant enzymes in human lung and liver. Preterm resuscitation with low oxygen causes less oxidative stress, inflammation, and chronic lung disease. Pediatrics — Prolonged moderate hyperoxia induced hyperresponsiveness and airway inflammation in newborn rats. Pediatr Res —9.

Free Radicals in Biology and Medicine. Oxford: Clarendon Press Turrens JF. Mitochondrial formation of reactive oxygen species.

An Introduction to Reactive Oxygen Species - Measurement of ROS in Cells

J Physiol Pt 2 — Sullivan JL. Am J Dis Child —4. Neonatal neutrophils: the good, the bad and the ugly. Clin Perinatol — Circulating xanthine oxidase: potential mediator of ischemic injury. Am J Physiol G— PubMed Abstract Google Scholar. The effect of hyperoxia on superoxide production by lung submitochondrial particles. Arch Biochem Biophys — O 2 sensing in hypoxic pulmonary vasoconstriction: the mitochondrial door re-opens.

Respir Physiol Neurobiol 1 — Cooper GM. The mechanism of oxidative phosphorylation. The Cell: A Molecular Approach. Sunderland, MA: Sinauer Associates Redox Biol — Iron species in iron homeostasis and toxicity. Analyst —7. Lefnesky EJ. Tissue iron overload and mechanisms of iron-catalyzed oxidative injury. Adv Exp Med Biol — Molecular mechanism of superoxide production by the mitochondrial respiratory chain.

Murphy MP. How mitochondria produce reactive oxygen species. Biochem J — Nox enzymes and new thinking on reactive oxygen: a double-edged sword revised. Annu Rev Pathol — Sies H. Role of reactive oxygen species in biological processes.