<p>Silk cultural relics, vital for global heritage studies, face preservation challenges from environmental metal ions. While prior work acknowledges metal ions’ role in silk degradation, the structural and chemical mechanisms of copper (Cu<sup>2+</sup>)-induced aging remain unresolved. This study systematically elucidates Cu<sup>2+</sup> impacts on artificially and historical silk using multimodal approaches, including SEM-EDS, XRD, FTIR, XPS, colourimeter, and amino acid analysis. Results reveal Cu<sup>2+</sup> triggers pitting, fibre fracture, and yellowing. β-sheet content declines sharply, transitioning to disordered α-helix/coil structures, paralleled by glycine, alanine, and serine depletion, corroborating crystallinity decline. Tyrosine loss in amorphous regions correlates with yellowing. Mechanistically, Cu<sup>2+</sup> mainly preferentially chelates histidine, aspartate, and glutamate via N/O coordination, initiating radical cascades that disrupt hydrogen bonding, accelerate oxidative and hydrolysis. This study establishes a structure-activity framework linking Cu<sup>2+</sup> contamination to silk degradation, offering molecular insights for preventive conservation. Multimodal methodology underscores the synergy of macro- and micro-scale analyses in heritage material research.</p>

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Mechanism of copper ion-induced degradation of silk cultural relics: a multimodal analytical approach

  • Xinying Hao,
  • Anan Wang,
  • Liya Ma,
  • Hongjin Li,
  • Biao Chen,
  • Meiying Li,
  • Li You,
  • Xinyu Shen

摘要

Silk cultural relics, vital for global heritage studies, face preservation challenges from environmental metal ions. While prior work acknowledges metal ions’ role in silk degradation, the structural and chemical mechanisms of copper (Cu2+)-induced aging remain unresolved. This study systematically elucidates Cu2+ impacts on artificially and historical silk using multimodal approaches, including SEM-EDS, XRD, FTIR, XPS, colourimeter, and amino acid analysis. Results reveal Cu2+ triggers pitting, fibre fracture, and yellowing. β-sheet content declines sharply, transitioning to disordered α-helix/coil structures, paralleled by glycine, alanine, and serine depletion, corroborating crystallinity decline. Tyrosine loss in amorphous regions correlates with yellowing. Mechanistically, Cu2+ mainly preferentially chelates histidine, aspartate, and glutamate via N/O coordination, initiating radical cascades that disrupt hydrogen bonding, accelerate oxidative and hydrolysis. This study establishes a structure-activity framework linking Cu2+ contamination to silk degradation, offering molecular insights for preventive conservation. Multimodal methodology underscores the synergy of macro- and micro-scale analyses in heritage material research.