The carbon dioxide/bicarbonate (CO₂/HCO₃^-) molecular pair is ubiquitous in mammalian cells and tissues, mainly as a result of oxidative decarboxylation reactions that occur during intermediary metabolism. CO₂ is in rapid equilibrium with HCO₃^- via the hydration reaction catalyzed by carbonic anhydrases. Far from being an inert compound in redox biology, CO₂ enhances or redirects the reactivity of peroxides, modulating the velocity, extent, and type of one- and two-electron oxidation reactions mediated by hydrogen peroxide (H₂O₂) and peroxynitrite (ONOO^-/ONOOH). Herein, we review the biochemical mechanisms by which CO₂ engages in peroxide-dependent reactions, free radical production, redox signaling, and oxidative damage. First, we cover the metabolic formation of CO₂ and its connection to peroxide formation and decomposition. Next, the reaction mechanisms, kinetics, and processes by which the CO₂/peroxide interplay modulates mammalian cell redox biology are scrutinized in-depth. Importantly, CO₂ also regulates gene expression related to redox and nitric oxide metabolism and as such influences oxidative and inflammatory processes. Accumulated biochemical evidence in vitro, in cellula, and in vivo unambiguously show that the CO₂ and peroxide metabolic pathways are intertwined and together participate in key redox events in mammalian cells.

二氧化碳/碳酸氢盐 (CO ₂ /HCO ₃ ^- ) 分子对在哺乳动物细胞和组织中普遍存在，主要是中间代谢过程中发生的氧化脱羧反应的结果。通过碳酸酐^酶催化的水合反应，CO ₂与 HCO _{3快速平衡。CO 2}远非氧化还原生物学中的惰性化合物，它增强或改变过氧化物的反应性，调节由过氧化氢 (H ₂ O ₂ ) 和过氧亚硝酸盐 ( H 2 O 2 ) 介导的一电子和二电子氧化反应的速度、程度和类型。小野^- /ONOOH）。在此，我们回顾了CO ₂参与过氧化物依赖性反应、自由基产生、氧化还原信号传导和氧化损伤的生化机制。首先，我们介绍了 CO ₂的代谢形成及其与过氧化物形成和分解的关系。接下来，深入研究CO ₂ /过氧化物相互作用调节哺乳动物细胞氧化还原生物学的反应机制、动力学和过程。重要的是，CO ₂还调节与氧化还原和一氧化氮代谢相关的基因表达，从而影响氧化和炎症过程。体外、细胞和体内积累的生化证据明确表明，CO ₂和过氧化物代谢途径相互交织，共同参与哺乳动物细胞中的关键氧化还原事件。