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Mitochondria are the main organelles that regulate energy metabolism in living organisms, as well as the primary organelle for the generation and elimination of reactive oxygen species. This report proposes that the protective role of H₂ may depend primarily on its unique ability to penetrate all aspects of cells and regulate mitochondrial homeostasis by activating the Keap1-Nrf2 phase II antioxidant system, rather than on its direct free radical scavenging activity. In this review, we summarize the protective effects and focus on the mechanism by which H₂ acts as a nutrient targeted to mitochondria through the activation of the Keap1-Nrf2 system in different disease models.

Molecular H₂ has been reported to have positive effects in the prevention and treatment of acute lung injury, chronic obstructive pulmonary disease, asthma, and pulmonary hypertension. It is interesting that the National Health Commission of China (NHC 7th edition trial: Beijing, 2020) and the Chinese Center for Disease Control and Prevention (CDCP 6th edition trial: Beijing, 2020) recommend effective O2 therapy as one of the modalities for the general treatment of patients with COVID-19. They also noted that inhalation of a mixture of molecular H2 and O2 (66.6% H2 and 33.3% O2) is more effective than inhalation of O2 alone. Research in our laboratory showed that enriched H2 and oxygenated saline inhibited LPS-induced lung injury in C57BL/6 mice via the NF-κB/NLRP3 signaling pathway. H2 demonstrated a more significant effect on inflammatory and anti-apoptotic mechanisms, while O2 potentiated the body's hypoxic effect, with the combined protective effect of the two gases being better than their individual effects.

Inhalation of 2% H2 improves mitochondrial function by increasing mitochondrial membrane potential and ATP levels, and promotes the activity of complex I and complex II of mitochondrial respiration. H2 also regulates mitochondrial dynamics, decreasing the expression of the mitochondrial fission protein Drp1 but increasing the expression of the mitochondrial fusion protein mitofusin-2 (MFN2).

Post-transplant morbidities, such as ischemia-reperfusion injury and graft-versus-host disease, are key challenges in transplantation. H2 acted as a prophylactic agent against post-transplant complications in several animal models of organ transplantation [74]. In a rat lung transplantation model, the combination of mechanical ventilation and prolonged cold ischemia resulted in a significant reduction in gas exchange in rat lung tissue (treatment with 98% O2 plus 2% nitrogen), while treatment with 98% O2 plus 2% H2 inhibited the increased expression of pro-inflammatory cytokines and apoptotic molecules and upregulated HO-1 expression in lung grafts. Furthermore, H2 molecules inhibited the levels of the pro-apoptotic proteins caspase-3 and caspase-8 in lung grafts, activated the expression of the anti-apoptotic proteins Bcl-2 and Bcl-xL, and stabilized the mitochondrial outer membrane, preventing the release of cytochrome c into the cytosol. In addition, advanced treatment of rat lung donors with H2 induces gene expression related to the stress response and ATP synthesis. H2 is considered a potential radioprotective agent. In the radiation-damaged A549 lung epithelial cell line, H2 negatively regulates the gene expression of pro-apoptotic Bax and inhibits its translocation to mitochondria through an unknown mechanism.

https://www.mdpi.com/2076-3921/12/12/2062?utm_source=chatgpt.com (2023)

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