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The interaction between hydrolytic and oxidative pathways in macrophage-mediated polyurethane degradation
Joanne E McBane1, J Paul Santerre, Rosalind S Labow
1Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.
Journal of Biomedical Materials Research. Part A
|March 6, 2007
Summary
Polycarbonate-based polyurethanes (PCNUs) degrade via combined hydrolytic and oxidative pathways mediated by macrophages. Pre-treating PCNUs with hydrogen peroxide (H2O2) alters degradation, highlighting the need to understand these mechanisms for biomaterial design.
Area of Science:
- Biomaterials Science
- Cell Biology
- Polymer Chemistry
Background:
- Polycarbonate-based polyurethanes (PCNUs) exhibit resistance to oxidation but are susceptible to degradation by monocyte-derived macrophages (MDM).
- Previous research indicated that hydrogen peroxide (H2O2) pretreatment influences PCNU degradation by esterases, suggesting a complex interplay of mechanisms.
- Understanding the dual hydrolytic and oxidative pathways is crucial for developing advanced biomaterials for in vivo applications.
Purpose of the Study:
- To elucidate the co-mediated hydrolytic and oxidative degradation mechanisms of PCNUs by human MDM.
- To investigate the effect of H2O2 pretreatment on PCNU degradation and MDM function.
- To correlate material surface chemistry with MDM-induced H2O2 release and degradation patterns.
Main Methods:
- Synthesis of 14C-radiolabeled PCNUs with varying stoichiometries (HDI431, HDI321) and a different diisocyanate (MDI321).
- Scanning electron microscopy (SEM) and radiolabel release measurements to assess PCNU degradation.
- Enzyme activity assays (esterase, acid phosphatase) and measurement of H2O2 release from MDM cultured on PCNU surfaces.
Main Results:
- H2O2 pretreatment of PCNU surfaces resulted in visible holes and increased radiolabel release, particularly for HDI431.
- MDM seeding on H2O2-treated PCNUs decreased degradation for HDI321 and MDI321, but not HDI431.
- Material surface chemistry influenced MDM-mediated H2O2 release, with HDI431 eliciting higher release, especially after phorbol myristate acetate (PMA) treatment.
Conclusions:
- PCNU degradation by MDM involves both hydrolytic and oxidative pathways, modulated by material chemistry and H2O2 pretreatment.
- H2O2 pretreatment alters the PCNU surface, impacting cell function and subsequent degradation.
- Tailoring PCNU surface chemistry is essential for controlling cell responses and optimizing biomaterial performance for in vivo use.
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