dc.rights.license | CC0 | en_US |
dc.contributor.author | Leveque, Clément | |
dc.contributor.author | Mrakic-Sposta, Simona | |
dc.contributor.author | Lafère, Pierre | |
dc.contributor.author | Vezzoli, Alessandra | |
dc.contributor.author | Germonpré, Peter | |
dc.contributor.author | Beer, Alexandre | |
dc.contributor.author | Mievis, Stéphane | |
dc.contributor.author | Virgili, Fabio | |
dc.contributor.author | LAMBRECHTS, Kate | |
dc.contributor.author | THEUNISSEN, Sigrid | |
dc.contributor.author | Guerrero, François | |
dc.contributor.author | BALESTRA, Costantino | |
dc.date.accessioned | 2023-10-09T14:27:53Z | |
dc.date.available | 2023-10-09T14:27:53Z | |
dc.date.issued | 2022-12-30 | |
dc.identifier.uri | https://luck.synhera.be/handle/123456789/2048 | |
dc.identifier.doi | https://doi.org/10.3390/ijms24010664 | en_US |
dc.description.abstract | Oxygen is a powerful trigger for cellular reactions and is used in many pathologies,
including oxidative stress. However, the effects of oxygen over time and at different partial pressures
remain poorly understood. In this study, the metabolic responses of normobaric oxygen intake
for 1 h to mild (30%) and high (100%) inspired fractions were investigated. Fourteen healthy nonsmoking subjects (7 males and 7 females; age: 29.9 ± 11.1 years, height: 168.2 ± 9.37 cm; weight:
64.4 ± 12.3 kg; BMI: 22.7 ± 4.1) were randomly assigned in the two groups. Blood samples were
taken before the intake at 30 min, 2 h, 8 h, 24 h, and 48 h after the single oxygen exposure. The level
of oxidation was evaluated by the rate of reactive oxygen species (ROS) and the levels of isoprostane.
Antioxidant reactions were observed by total antioxidant capacity (TAC), superoxide dismutase
(SOD), and catalase (CAT). The inflammatory response was measured using interleukin-6 (IL-6),
neopterin, creatinine, and urates. Oxidation markers increased from 30 min on to reach a peak at 8 h.
From 8 h post intake, the markers of inflammation took over, and more significantly with 100% than
with 30%. This study suggests a biphasic response over time characterized by an initial “permissive
oxidation” followed by increased inflammation. The antioxidant protection system seems not to be
the leading actor in the first place. The kinetics of enzymatic reactions need to be better studied to
establish therapeutic, training, or rehabilitation protocols aiming at a more targeted use of oxygen. | en_US |
dc.description.abstractfr | Oxygen is a powerful trigger for cellular reactions and is used in many pathologies,
including oxidative stress. However, the effects of oxygen over time and at different partial pressures
remain poorly understood. In this study, the metabolic responses of normobaric oxygen intake
for 1 h to mild (30%) and high (100%) inspired fractions were investigated. Fourteen healthy nonsmoking subjects (7 males and 7 females; age: 29.9 ± 11.1 years, height: 168.2 ± 9.37 cm; weight:
64.4 ± 12.3 kg; BMI: 22.7 ± 4.1) were randomly assigned in the two groups. Blood samples were
taken before the intake at 30 min, 2 h, 8 h, 24 h, and 48 h after the single oxygen exposure. The level
of oxidation was evaluated by the rate of reactive oxygen species (ROS) and the levels of isoprostane.
Antioxidant reactions were observed by total antioxidant capacity (TAC), superoxide dismutase
(SOD), and catalase (CAT). The inflammatory response was measured using interleukin-6 (IL-6),
neopterin, creatinine, and urates. Oxidation markers increased from 30 min on to reach a peak at 8 h.
From 8 h post intake, the markers of inflammation took over, and more significantly with 100% than
with 30%. This study suggests a biphasic response over time characterized by an initial “permissive
oxidation” followed by increased inflammation. The antioxidant protection system seems not to be
the leading actor in the first place. The kinetics of enzymatic reactions need to be better studied to
establish therapeutic, training, or rehabilitation protocols aiming at a more targeted use of oxygen. | en_US |
dc.description.abstracten | Oxygen is a powerful trigger for cellular reactions and is used in many pathologies,
including oxidative stress. However, the effects of oxygen over time and at different partial pressures
remain poorly understood. In this study, the metabolic responses of normobaric oxygen intake
for 1 h to mild (30%) and high (100%) inspired fractions were investigated. Fourteen healthy nonsmoking subjects (7 males and 7 females; age: 29.9 ± 11.1 years, height: 168.2 ± 9.37 cm; weight:
64.4 ± 12.3 kg; BMI: 22.7 ± 4.1) were randomly assigned in the two groups. Blood samples were
taken before the intake at 30 min, 2 h, 8 h, 24 h, and 48 h after the single oxygen exposure. The level
of oxidation was evaluated by the rate of reactive oxygen species (ROS) and the levels of isoprostane.
Antioxidant reactions were observed by total antioxidant capacity (TAC), superoxide dismutase
(SOD), and catalase (CAT). The inflammatory response was measured using interleukin-6 (IL-6),
neopterin, creatinine, and urates. Oxidation markers increased from 30 min on to reach a peak at 8 h.
From 8 h post intake, the markers of inflammation took over, and more significantly with 100% than
with 30%. This study suggests a biphasic response over time characterized by an initial “permissive
oxidation” followed by increased inflammation. The antioxidant protection system seems not to be
the leading actor in the first place. The kinetics of enzymatic reactions need to be better studied to
establish therapeutic, training, or rehabilitation protocols aiming at a more targeted use of oxygen. | en_US |
dc.description.sponsorship | COM | en_US |
dc.language.iso | EN | en_US |
dc.publisher | MDPI | en_US |
dc.relation.ispartof | International Journal of Molecular sciences | en_US |
dc.rights.uri | Open access | en_US |
dc.subject | normobaric oxygen paradox | en_US |
dc.subject | hyperoxic–hypoxic paradox | en_US |
dc.subject | hyperoxia | en_US |
dc.subject | oxygen biology | en_US |
dc.subject | cellular reactions | en_US |
dc.subject | human | en_US |
dc.subject | oxygen therapy | en_US |
dc.subject | human performance | en_US |
dc.subject | decompression | en_US |
dc.subject | diving | en_US |
dc.subject.fr | Hyperoxie | en_US |
dc.subject.en | Normobaric Oxygen Paradox | en_US |
dc.subject.en | hyperoxic–hypoxic paradox | en_US |
dc.subject.en | Hyperoxie | en_US |
dc.subject.en | oxygen biology | en_US |
dc.subject.en | cellular reactions | en_US |
dc.subject.en | human | en_US |
dc.subject.en | oxygen therapy | en_US |
dc.subject.en | human performance | en_US |
dc.subject.en | decompression | en_US |
dc.subject.en | diving | en_US |
dc.title | Oxidative Stress Response’s Kinetics after 60 Minutes at Different (30% or 100%) Normobaric Hyperoxia Exposures | en_US |
dc.title.en | Oxidative Stress Response’s Kinetics after 60 Minutes at Different (30% or 100%) Normobaric Hyperoxia Exposures | en_US |
dc.title.fr | Oxidative Stress Response’s Kinetics after 60 Minutes at Different (30% or 100%) Normobaric Hyperoxia Exposures | en_US |
dc.type | Article scientifique | en_US |
synhera.classification | Sciences de la santé humaine | en_US |
synhera.institution | HE Bruxelles Brabant | en_US |
synhera.stakeholders.fund | DELTO2X Project | en_US |
synhera.cost.total | 3000 | en_US |
synhera.cost.apc | 3000 | en_US |
synhera.cost.comp | 0 | en_US |
synhera.cost.acccomp | 0 | en_US |
dc.description.version | Oui | en_US |
dc.rights.holder | Les auteurs | en_US |