The effect of oxygen on the lung

Claireaux, A. E.

doi:10.1136/jcp.28.suppl_9.75

Cited by 8 publications

(2 citation statements)

References 18 publications

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“…In the presence of SP, both edema and inflammatory cell infiltration were reduced despite exposure to hyperoxia; there was no significant histopathologic difference between normoxia/saline and normoxia/SP groups ( Figure 1C). In addition, the lung injury scores in hyperoxia/SP rats were significantly lower than those of hyperoxia/saline rats (hyperoxia: F [1,20] …”

Section: Sp Reduced Hyperoxic Lung Injury and Lung Edema Induced By Hmentioning

confidence: 98%

“…Supplement of very high concentrations of oxygen is required to maintain sufficient blood oxygenation in the patients, which can lead to the development of chronic lung disease in infancy, also known as bronchopulmonary dysplasia (BPD) [1,2]. In recent years, reactive oxygen species (ROS) generated during hyperoxic insult have been generally accepted to play a critical role in lung injury [3].…”

Section: Introductionmentioning

confidence: 99%

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Substance P protects against hyperoxic-induced lung injury in neonatal rats

Huang

Shuhong

et al. 2014

Experimental Lung Research

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The aim of the study was to investigate the effects of substance P (SP) in hyperoxia-induced lung injury in newborn rats. Thirty-two rat pups were randomly divided into four groups: normoxia/saline, normoxia/SP, hyperoxia/saline and hyperoxia/SP. In a separate set of experiments, the neonatal rat pups were exposed to 21% or >95% O2 for 14 days with or without intraperitoneal administration of SP. On day 14, the animals were sacrificed and the lungs were processed for histology and biochemical analysis. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was used for the detection of apoptosis. Antioxidant capacity was assessed by glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), oxidative stress was assessed by determining the extent of formation of malondialdehyde (MDA), activities of NADPH oxidase activity, and formation of reactive oxygen species (ROS). The activity of phospho-p38 (p-p38) and -ERK1/2 (p-ERK1/2) proteins and expression of NF-E2-related factor 2 (NRF2) were detected by Western blot, and the expression of p-p38 was detected by immunofluorescence analysis. Compared with the hyperoxia treatment, the lung damage was significantly ameliorated following the SP treatment. Furthermore, the lungs from the pups exposed to hyperoxia TUNEL-positive nuclei increased markedly and decreased significantly after SP treatment. The levels of MDA decreased and that of GSH-Px and SOD increased following the SP treatment. The SP treatment significantly suppressed the activity of NADPH oxidase and reduced ROS production. SP stimulation may result in blocking p38 MAPK and ERK signaling pathways, and the activities of p-p38 and p-ERK, and expression of NRF2 decreased following the SP treatment. These findings indicate that SP can ameliorate hyperoxic lung injury through decreasing cell apoptosis, elevating antioxidant activities, and attenuating oxidative stress.

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Section: Sp Reduced Hyperoxic Lung Injury and Lung Edema Induced By Hmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Substance P protects against hyperoxic-induced lung injury in neonatal rats

Huang

Shuhong

et al. 2014

Experimental Lung Research

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Hyperbaric Environment: Oxygen and Cellular Damage versus Protection

Poff

Kernagis

D’Agostino

2016

Comprehensive Physiology

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The elevation of tissue pO2 induced by hyperbaric oxygen (HBO) is a physiological stimulus that elicits a variety of cellular responses. These effects are largely mediated by, or in response to, an increase in the production of reactive oxygen and nitrogen species (RONS). The major consequences of elevated RONS include increased oxidative stress and enhanced antioxidant capacity, and modulation of redox-sensitive cell signaling pathways. Interestingly, these phenomena underlie both the therapeutic and potentially toxic effects of HBO. Emerging evidence indicates that supporting mitochondrial health is a potential method of enhancing the therapeutic efficacy of, and preventing oxygen toxicity during, HBO. This review will focus on the cellular consequences of HBO, and explore how these processes mediate a delicate balance of cellular protection versus damage. © 2017 American Physiological Society. Compr Physiol 7:213-234, 2017.

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