Intermittent hyperbaric oxygen exposure mobilizing peroxiredoxin 6 to prevent oxygen toxicity

Abstract

Intermittent hyperbaric oxygen exposure (IE-HBO) can protect the body against oxygen toxicity, but the underlying mechanisms are not very clear. Peroxiredoxin 6 (Prdx6) is a special endogenous antioxidative protein. We explored if the protective effects of IE-HBO are related to Prdx6. Mice were exposed to 280 kPa O 2 for 60 min, followed by 30-min exposure to 20% O 2 /N 2 mixture with equal pressure, repeated for six cycles. The Prdx6 protein level and non-selenium glutathione peroxidase (NSGPx) activity in the brain and lungs were then measured and the injury degree of lung and the oxidation level of brain and lung were evaluated. On this basis, the relationship between Prdx6 and IE-HBO's protection was explored. Generally, both IE-HBO and continuous exposure to HBO (CE-HBO) could increase the protein and mRNA levels of Prdx6, and such increases were more significant 24 h after cessation of exposure; moreover, the Prdx6 level of IE-HBO was higher than that of CE-HBO in both brain and lung, also more significantly 24 h after cessation of exposure. In addition, IE-HBO exposure could more effectively potentiate the activity of NSGPx and increase GSH content in brain and lung tissues. At the same time, it could reduce oxidation products in these tissues. IE-HBO could also provide protection for the lungs against injuries resulting from prolonged HBO exposure. These data showed that IE-HBO can potentiate the production and the activity of Prdx6 and consequently mitigate oxidative damages in brain and lungs. The influences of IE-HBO on Prdx6 may form an important basis for its protection against oxygen toxicity.

Pulmonary Oxygen Toxicity Through Exhaled Breath Markers After Hyperbaric Oxygen Treatment Table 6

“…POT and CNS-OT in rodents may be reduced when a period with greatly increased partial pressure for oxygen is followed by a lower partial oxygen pressure or even a normoxic period at constant ambient pressure ( Arieli and Gutterman, 1997 ; Chavko et al, 2008 ). This protective effect at similar total oxygen exposure times was greater when alternating hyperoxic-normoxic schedules were more rather than less frequent ( Arieli and Gutterman, 1997 ; Zhang et al, 2019 ). These findings suggest that the incidence of POT would be lower with our modified TT6, with more frequently alternating oxygen-air periods at 9 m, than with the original US Navy TT6.…”

Can hyperbaric oxygen safely serve as an anti-inflammatory treatment for COVID-19?

“…Acute severe toxicity is normally only seen in hyperbaric settings >200 kPa and include CNS toxicity presenting as blurred vision and in worst case self-limiting seizures [44] , occurring in < 1/10.000 treatments. Paradoxically intermittent HBO 2 has also been shown to protect lungs against oxygen toxicity by upregulation of anti-oxidative factors [45] , [46] . Even though concerns of pulmonary toxicity are theoretical for the proposed treatment duration [47] , the extent of COVID-19 pathology is unknown and potential toxic effect of oxygen should be monitored in a randomized clinical trial.…”

An Extra Breath of Fresh Air: Hyperbaric Oxygenation as a Stroke Therapeutic

“…Effective ischemic tolerance can be developed when dosed with HBOT for 3–5 days [ 91 , 135 ]. Although, HBOT also induced neuroprotection against brain injuries, due to ischemia during a certain time frame [ 94 ], neuroprotection was achieved through biphasic time frames characterized by instant and delayed preconditioning effect [ 42 , 140 ]. Instantaneous preconditioning was evident within the first hour after treatment, demonstrating alterations in ion channel activities, enzyme activity, and secondary messengers [ 140 ].…”

“…Although, HBOT also induced neuroprotection against brain injuries, due to ischemia during a certain time frame [ 94 ], neuroprotection was achieved through biphasic time frames characterized by instant and delayed preconditioning effect [ 42 , 140 ]. Instantaneous preconditioning was evident within the first hour after treatment, demonstrating alterations in ion channel activities, enzyme activity, and secondary messengers [ 140 ]. On the other hand, delayed preconditioning involved cellular changes that progressed slower and developed enduring changes in gene and protein expression [ 140 ].…”

“…Instantaneous preconditioning was evident within the first hour after treatment, demonstrating alterations in ion channel activities, enzyme activity, and secondary messengers [ 140 ]. On the other hand, delayed preconditioning involved cellular changes that progressed slower and developed enduring changes in gene and protein expression [ 140 ].…”