TABLE 3.
The effect of hyperoxia on aging markers in rats.
| Author and year | Condition | Age | Hyperoxia protocol | Aging markers | Results | Conclusion | Safety issues |
|---|---|---|---|---|---|---|---|
| Hosford, (2003) | Healthy | 4–14 days | >95% O2 for 10 days | VEGF | mRNA levels of VEGF increased in normoxic animals, but hyperoxia suppressed this increase | Hyperoxic exposure decreased VEGF levels, and decreased VEGF receptors (VEGFR1 and VEGFR2) levels | Not reported |
| VEGF receptors (VEGFR1 and EGFR2) | VEGFR1 and VEGFR2 mRNA increased in normoxic animals, but they were decreased by hyperoxia | ||||||
| HIF-2 α | mRNA levels of HIF-2 α increased in normoxic animals, but hyperoxia suppressed this increase | ||||||
| Shwe et al. (2021) | NA | >20 weeks | 100% O2 at 2 ATA for 80 min/day for 14 days | Synaptic plasticity [Markers: LTD, LTP, dendritic spine density, expression of synaptic protein (PSD 95)] | Synaptic plasticity was restored/improved | HBOT attenuated insulin resistance, cognitive impairment, hippocampal aging and pathologies. These findings suggest that HBOT restored insulin sensitivity, hippocampal functions, cognition in aging, and aging-obese models | Not reported |
| Hippocampal insulin receptor function (marker: LTD) | Insulin receptor function was restored/improved | ||||||
| Hippocampal ROS level | ROS was decreased | ||||||
| DCX | Could not restore neurogenesis | ||||||
| Hippocampal autophagy (markers: p62 and LC3-II) | Hippocampal autophagy was restored | ||||||
| Microglia hyperactivation | Microglial hyperactivation was attenuated | ||||||
| Hippocampal apoptosis | Hippocampal apoptosis reversed back to normal | ||||||
| Aging marker: beta-secretase (BACE1) | BACE1 enzyme was reduced | ||||||
| Aging marker: telomere length | Telomere length was restored | ||||||
| Aging marker: SA-β-gal staining | The number of SA-β-gal-positive cells was decreased | ||||||
| Zhang et al. (2010) | Healthy | 2–14 months | 60% O2 for 3 weeks | mtDNA damage | Increased | These data emphasize the importance of DNA repair enzymes and antioxidant enzymes as targets to promote DNA repair and reduce production of ROS. | Increasing the exposure of the lens to hyperoxia could lead to mtDNA damage and increase the risk of nuclear cataract formation |
| mtBER enzymes | Increased | ||||||
| 8-OHdG levels | Increased |
NM, not mentioned; VEGF, Vascular endothelial growth factor; LTD, Insulin-induced long-term depression; LTP, long-term potentiation; SA-β-gal, senescence-associated β falactosidase; DCFHDA, dichloro-hydrofluoresceindiacetate; DCX, neurogenesis; mtBER, mtDNA, base excision repair; mtDNA, mitochondrial DNA; LX-PCR, Long extension polymerase chain reaction; 8-OHdG, 8-hydroxy-20-deoxy-guanosine.