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Oxygen toxicity: cellular mechanisms in normobaric hyperoxia
Cell Biology and Toxicology ( IF 6.1 ) Pub Date : 2022-09-16 , DOI: 10.1007/s10565-022-09773-7
Ricardo Alva 1 , Maha Mirza 1 , Adam Baiton 1 , Lucas Lazuran 1 , Lyuda Samokysh 1 , Ava Bobinski 1 , Cale Cowan 1 , Alvin Jaimon 1 , Dede Obioru 1 , Tala Al Makhoul 1 , Jeffrey A Stuart 1
Affiliation  

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.

Graphical abstract

• Hyperoxia promotes overproduction of reactive oxygen species (ROS).

• Hyperoxia dysregulates a variety of signaling pathways, such as the Nrf2, NF-κB and MAPK pathways.

• Hyperoxia causes cell death by multiple pathways.

• Antioxidants, particularly, mitochondria-targeted antioxidants, have shown promising results as therapeutic agents against oxygen toxicity in animal models.



中文翻译:

氧中毒:常压高氧的细胞机制

在临床环境中,氧疗适用于早产新生儿和患有急性和慢性疾病(例如 COVID-19、肺纤维化、败血症、心脏骤停、一氧化碳中毒和急性心力衰竭)的成人。在非临床环境中,潜水员和宇航员也可能接受补充氧气。此外,根据目前的标准细胞培养实践,细胞维持在大气中的氧气中,这比大多数细胞在体内所经历的要高几倍。在上述所有情况下,氧气水平升高(高氧)会导致线粒体、NADPH 氧化酶和其他来源的活性氧的产生增加。这会导致细胞功能障碍或死亡。急性高氧损伤会损害各种细胞功能,最终表现为生理缺陷。慢性高氧,特别是在新生儿中,会破坏发育,导致永久性缺陷。在这篇综述中,我们讨论了受高氧影响的细胞活动和通路,以及为改善损伤而开发的策略。

图形概要

• 高氧促进活性氧(ROS) 的过量产生。

• 高氧会失调多种信号通路,例如Nrf2、NF-κB 和MAPK 通路。

• 高氧通过多种途径导致细胞死亡。

• 抗氧化剂,尤其是靶向线粒体的抗氧化剂,在动物模型中作为抗氧中毒的治疗剂显示出可喜的结果。

更新日期:2022-09-16
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