Hypochlorous acid (HOCl) is a potent cytotoxic oxidant generated by the enzyme myeloperoxidase (MPO) in the presence of hydrogen peroxide (H₂O₂) and chloride (Cl⁻). Elevated levels of HOCl play an important role in various pathological conditions through oxidative modification of several biomolecules. Recently, we have highlighted the ability of HOCl to mediate the destruction of the metal‐ion derivatives of tetrapyrrole macrocyclic rings such as hemoproteins and vitamin B₁₂ (VB₁₂) derivatives. Destruction of cyanocobalamin, a common pharmacological form of VB₁₂ mediated by HOCl, results in the generation of toxic molecular products such as chlorinated derivatives, corrin ring cleavage products, the toxic blood agents cyanide (CN⁻) and cyanogen chloride (CNCl), and redox‐active free cobalt. Here, we show that melatonin prevents HOCl‐mediated cyanocobalamin destruction, using a combination of UV‐Vis spectrophotometry, high‐performance liquid chromatography analysis, and colorimetric CNCl assay. Identification of several melatonin oxidation products suggests that the protective role of melatonin against HOCl‐mediated cyanocobalamin destruction and subsequent CNCl generation is at the expense of melatonin oxidation. Collectively, this work highlights that, in addition to acting as an antioxidant and as a MPO inhibitor, melatonin can also prevent VB₁₂ deficiency in inflammatory conditions such as cardiovascular and neurodegenerative diseases, among many others.

中文翻译：

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褪黑素可防止次氯酸介导的氰钴胺素的破坏和氯化氰的生成

次氯酸（HOCl）在过氧化氢（H存在下由髓过氧化物酶（MPO）产生的有效的细胞毒性氧化剂₂ ö ₂）和氯（氯^- ）。HOCl的水平升高通过多种生物分子的氧化修饰在各种病理状况中起重要作用。最近，我们强调了HOCl介导四吡咯大环金属离子衍生物（如血蛋白和维生素B ₁₂（VB ₁₂）衍生物）破坏的能力。破坏氰钴胺素，VB _12的一种常见药理形式通过次氯酸介导的，导致有毒分子产物的产生，如氯代衍生物，咕啉环的裂解产物，毒性血剂氰化物（CN ^- ）和氯化氰（CNCL），和氧化还原活性不含钴。在这里，我们证明了褪黑素通过结合使用紫外可见分光光度法，高效液相色谱分析和比色CNC1分析可防止HOCl介导的氰钴胺素的破坏。对几种褪黑激素氧化产物的鉴定表明，褪黑激素对HOCl介导的氰基钴胺素破坏和随后的CNCl生成的保护作用是以褪黑激素氧化为代价的。总的来说，这项工作突出表明，褪黑激素除了作为抗氧化剂和MPO抑制剂外，还可以预防VB _12。 炎症性疾病的缺乏，例如心血管疾病和神经退行性疾病等。