Hydrogen molecule (H₂) exhibits broad-spectrum but microenvironment-dependent biomedical effects in varied oxidation stress-related diseases, but its molecular mechanism is unclear and its targeting molecule is unknown so far. Herein, we originally reveal that Fe-porphyrin is a H₂-targeted molecule. We have demonstrated that the oxidized Fe-porphyrin in both free and protein-confining states can self-catalyze the hydrogenation/reduction by reacting with H₂ to catalytically scavenge ·OH, and can also catalytically hydrogenate to reduce CO₂ into CO in the hypoxic microenvironment of in vitro simulation and in vivo tumor, confirming that Fe-porphyrin is a redox-related biosensor of H₂ and H₂ is an upstream signaling molecule of CO. These discoveries are favorable for deep understanding and exploration of profound biomedical effects of H₂, and helpful for development of innovative drugs and hydrogen energy/agricultural materials.

氢分子（H ₂）在多种氧化应激相关疾病中表现出广谱但微环境依赖性的生物医学作用，但其分子机制尚不清楚，其靶向分子目前尚不清楚。在此，我们最初揭示了Fe-卟啉是一种H ₂靶向分子。我们已经证明，游离态和蛋白质限制态的氧化铁卟啉可以通过与H ₂反应自催化加氢/还原以催化清除·OH，也可以在缺氧状态下催化加氢将CO _2还原为CO体外模拟和体内肿瘤微环境，证实铁卟啉是H的氧化还原相关生物传感器₂和H ₂是CO的上游信号分子。这些发现有利于深入理解和探索H ₂的深刻生物医学效应，有助于创新药物和氢能/农用材料的开发。