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<p>316L stainless steel (SS) is commonly used in medical implants due to its outstanding mechanical properties and biocompatibility. However, increasing use of metallic implants has raised concerns about microbiologically influenced corrosion (MIC) in intestinal environments. This study presents the first evidence that <i>Listeria monocytogenes</i> can induce significant MIC on 316L SS under simulated intestinal conditions. <i>L. monocytogenes</i> forms dense biofilms on metal surfaces, accelerating corrosion and causing severe pitting. Corrosion rates are further heightened under carbon starvation, indicating extracellular electron transfer (EET) involvement. Electrochemical analyses reveal that <i>L. monocytogenes</i> disrupts the protective oxide layer via a riboflavin-mediated EET pathway. Riboflavin intensifies corrosion by enhancing electron transfer between bacteria and metal surfaces. These results highlight the critical role of EET in <i>L. monocytogenes</i>-induced MIC and provide new insights into corrosion mechanisms of metallic implants in intestinal environments, laying the foundations for developing corrosion-resistant biomaterials and protective strategies.</p>

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Riboflavin-mediated extracellular electron transfer enhances microbiologically influenced corrosion of 316L stainless steel by Listeria monocytogenes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月17日

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  • Xiaomeng Liu,
  • Yongqiang Fan,
  • Fuhui Wang,
  • Dake Xu

摘要

316L stainless steel (SS) is commonly used in medical implants due to its outstanding mechanical properties and biocompatibility. However, increasing use of metallic implants has raised concerns about microbiologically influenced corrosion (MIC) in intestinal environments. This study presents the first evidence that Listeria monocytogenes can induce significant MIC on 316L SS under simulated intestinal conditions. L. monocytogenes forms dense biofilms on metal surfaces, accelerating corrosion and causing severe pitting. Corrosion rates are further heightened under carbon starvation, indicating extracellular electron transfer (EET) involvement. Electrochemical analyses reveal that L. monocytogenes disrupts the protective oxide layer via a riboflavin-mediated EET pathway. Riboflavin intensifies corrosion by enhancing electron transfer between bacteria and metal surfaces. These results highlight the critical role of EET in L. monocytogenes-induced MIC and provide new insights into corrosion mechanisms of metallic implants in intestinal environments, laying the foundations for developing corrosion-resistant biomaterials and protective strategies.