Oxygen toxicity: simultaneous measure of pentane and malondialdehyde in humans exposed to hyperoxia

Loiseaux-Meunier, Marie-Nadia; Boccadoro, Mario; Gentou, C; Pépin, D.; Coudert, J; Caillaud, D.

doi:10.1016/s0753-3322(01)00042-7

Cited by 39 publications

(27 citation statements)

References 26 publications

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“…Changes in VOC were also found after hyperoxic exposure [69,84,89,90]. The changes in VOC most frequently observed after normobaric hyperoxia were an increase in pentane and methyl alkanes [84,89,90], while the VOC breath print found after submersed hyperoxia consists mainly of methyl alkanes [69]. In the latter study, because changes in VOC were found 4 h post-exposure, the pathophysiological background could be either a primarily lipid peroxidation-induced pathway or a delayed inflammatory one.…”

Section: Future Perspectives In Monitoring Potmentioning

confidence: 77%

“…Breath prints have been identified that can be used for the assessment of diseases like lung cancer [82][83][84], infectious diseases like tuberculosis [85], and inflammatory conditions such as asthma [86,87] and COPD [87,88]. Changes in VOC were also found after hyperoxic exposure [69,84,89,90]. The changes in VOC most frequently observed after normobaric hyperoxia were an increase in pentane and methyl alkanes [84,89,90], while the VOC breath print found after submersed hyperoxia consists mainly of methyl alkanes [69].…”

Section: Future Perspectives In Monitoring Potmentioning

confidence: 99%

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Oxygen, the lung and the diver: friends and foes?

2016

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Worldwide, the number of professional and sports divers is increasing. Most of them breathe diving gases with a raised partial pressure of oxygen (PO 2 ). However, if the PO 2 is between 50 and 300 kPa (375-2250 mmHg) (hyperoxia), pathological pulmonary changes can develop, known as pulmonary oxygen toxicity (POT). Although in its acute phase, POT is reversible, it can ultimately lead to non-reversible pathological changes. Therefore, it is important to monitor these divers to prevent them from sustaining irreversible lesions.This review summarises the pulmonary pathophysiological effects when breathing oxygen with a PO 2 of 50-300 kPa (375-2250 mmHg). We describe the role and the limitations of lung function testing in monitoring the onset and development of POT, and discuss new techniques in respiratory medicine as potential markers in the early development of POT in divers. @ERSpublications To prevent the early development of pulmonary oxygen toxicity divers must be properly monitored

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Section: Future Perspectives In Monitoring Potmentioning

confidence: 77%

Section: Future Perspectives In Monitoring Potmentioning

confidence: 99%

Oxygen, the lung and the diver: friends and foes?

2016

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“…Hyperoxia in normal humans breathing 100% oxygen has been reported to increase breath levels of pentane as well as serum malondialdehyde [9,10] but induced hyperoxia in newborn lambs elicited no significant changes in either breath ethane or pentane [17]. In preterm infants ventilated for respiratory distress syndrome, DRURY et al [18] found no correlation between fractional inspired oxygen concentration and exhaled pentane, but NYCYK et al [19] found an association between high-peak pentane exhalation and low gestational age, mortality, intraventricular haemorrhage and retinopathy of prematurity.…”

Section: Discussionmentioning

confidence: 99%

“…There is little evidence that this is beneficial and it may potentially be harmful by inducing an increase in oxidative stress. However, the effects of oxygen on markers of oxidative stress have not been totally elucidated because previous studies have yielded conflicting results [9][10][11][12]. The current authors have recently reported a sensitive new index of oxidative stress, the breath methylated alkane contour (BMAC), comprising a three-dimensional surface plot of the abundance in breath of C4-C20 alkanes and their monomethylated derivatives [13].…”

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confidence: 99%

Effect of oxygen on breath markers of oxidative stress

Phillips¹,

Cataneo²,

Greenberg³

et al. 2002

Eur Respir J

111

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Supplemental oxygen is often administered to induce hyperoxia in nonhypoxic patients for indications such as chest pain, despite lack of evidence of clinical benefit. Induced hyperoxia is potentially toxic, since it may increase oxidative stress and peroxidative damage to deoxyribonucleic acid, lipids and proteins.The aim of this study was to establish whether supplemental oxygen induces oxidative stress in nonhypoxic subjects.Breath markers of oxidative stress were measured in 31 healthy subjects before and after breathing 28% oxygen at 2.0 L?min -1 via nasal prongs for 30 min while resting. The criterion standard of oxidative stress was the breath methylated alkane contour (BMAC), a three-dimensional plot of the alveolar gradients of C4-C20 alkanes and monomethylated alkanes produced by lipid peroxidation. Volatile organic compounds (VOCs) in breath were assayed by gas chromatography and mass spectroscopy, and the BMACs before and after oxygenation were compared.Following oxygenation, there was a significant increase in mean volume under the curve of the BMAC and in alveolar gradients of three VOCs: 3-methyltridecane, 3-methylundecane and 5-methylnonane.Breath markers of oxidative stress were significantly increased in normal volunteers breathing supplemental oxygen for 30 min.

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“…First, hyperoxia and fluctuations in inhaled oxygen content can produce severe retinopathy in preterm infants and newborn rodents (30,31). Second, stepped increases in inhaled oxygen concentration produce acute increases in exhaled biomarkers of oxidative stress (32)(33)(34) and in a marker of airway inflammation (34). Third, there is growing appreciation that oxidative stress may contribute to the progression of COPD through stimulation of many molecular pathways that are believed to be involved in COPD pathogenesis (35).…”

Section: Reasons For Patients With Copd Not To Receive Ltotmentioning

confidence: 99%

Long-term Oxygen Treatment in Chronic Obstructive Pulmonary Disease: Recommendations for Future Research

Croxton

Bailey

2006

Am J Respir Crit Care Med

166

109

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Long-term oxygen treatment (LTOT) prolongs life in patients with chronic obstructive pulmonary disease (COPD) and severe resting hypoxemia. Although this benefit is proven by clinical trials, scientific research has not provided definitive guidance regarding who should receive LTOT and how it should be delivered. Deficiencies in knowledge and in current research activity related to LTOT are especially striking in comparison to the importance of LTOT in the management of COPD and the associated costs. The National Heart, Lung, and Blood Institute, in collaboration with the Centers for Medicare and Medicaid Services, convened a working group to discuss research on LTOT. Participants in this meeting identified specific areas in which further investigation would likely lead to improvements in the care of patients with COPD or reductions in the cost of their care. The group recommended four clinical trials in subjects with COPD: (1 ) efficacy of ambulatory O 2 supplementation in subjects who experience oxyhemoglobin desaturation during physical activity but are not severely hypoxemic at rest; (2 ) efficacy of LTOT in subjects with severe COPD and only moderate hypoxemia; (3 ) efficacy of nocturnal O 2 supplementation in subjects who show episodic desaturation during sleep that is not attributable to obstructive sleep apnea; and (4 ) effectiveness of an activitydependent prescription for O 2 flow rate that is based on clinical tests performed at rest, during exercise, and during sleep.

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Oxygen toxicity: simultaneous measure of pentane and malondialdehyde in humans exposed to hyperoxia

Cited by 39 publications

References 26 publications

Oxygen, the lung and the diver: friends and foes?

Oxygen, the lung and the diver: friends and foes?

Effect of oxygen on breath markers of oxidative stress

Long-term Oxygen Treatment in Chronic Obstructive Pulmonary Disease: Recommendations for Future Research

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