Oxygen toxicity: cellular mechanisms in normobaric hyperoxia

被引：68

作者：

Alva, Ricardo ^{[1
]}

Mirza, Maha ^{[1
]}

Baiton, Adam ^{[1
]}

Lazuran, Lucas ^{[1
]}

Samokysh, Lyuda ^{[1
]}

Bobinski, Ava ^{[1
]}

Cowan, Cale ^{[1
]}

Jaimon, Alvin ^{[1
]}

Obioru, Dede ^{[1
]}

Al Makhoul, Tala ^{[1
]}

Stuart, Jeffrey A. ^{[1
]}

机构：

[1] Brock Univ, Dept Biol Sci, St Catharines, ON L2S 3A1, Canada

来源：

CELL BIOLOGY AND TOXICOLOGY | 2023年 / 39卷 / 01期

基金：

加拿大自然科学与工程研究理事会;

关键词：

Hyperoxia; Reactive oxygen species; Oxygen toxicity; Mitochondria; Cell death; Antioxidants; INDUCED LUNG INJURY; NF-KAPPA-B; INNER MITOCHONDRIAL-MEMBRANE; CYTOCHROME-C RELEASE; PROLYL HYDROXYLASE INHIBITION; HYPOXIA-INDUCIBLE FACTOR; LONG NONCODING RNAS; OXIDATIVE STRESS; PERMEABILITY TRANSITION; BRONCHOPULMONARY DYSPLASIA;

D O I：

10.1007/s10565-022-09773-7

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

In clinical settings, oxygen therapy is administered to preterm neonates and to adults with acute and chronic conditions such as COVID-19, pulmonary fibrosis, sepsis, cardiac arrest, carbon monoxide poisoning, and acute heart failure. In non-clinical settings, divers and astronauts may also receive supplemental oxygen. In addition, under current standard cell culture practices, cells are maintained in atmospheric oxygen, which is several times higher than what most cells experience in vivo. In all the above scenarios, the elevated oxygen levels (hyperoxia) can lead to increased production of reactive oxygen species from mitochondria, NADPH oxidases, and other sources. This can cause cell dysfunction or death. Acute hyperoxia injury impairs various cellular functions, manifesting ultimately as physiological deficits. Chronic hyperoxia, particularly in the neonate, can disrupt development, leading to permanent deficiencies. In this review, we discuss the cellular activities and pathways affected by hyperoxia, as well as strategies that have been developed to ameliorate injury.

引用

页码：111 / 143

页数：33

共 355 条

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