BACKGROUND: Treatment of actinide-contaminated wounds may be problematic because of contaminant physicochemical properties, dissemination and anatomical localization. This study investigates different chelation/resection protocols after contamination of rats with americium (Am) or plutonium (Pu) nitrate or mixed oxide (MOX; uranium (U), Pu oxide). METHODS: Anesthetized rats were contaminated with Am or Pu nitrate (moderately soluble) or MOX (insoluble) following wounding of hind leg muscle. DTPA (diethylene triamine pentaacetic acid) treatment (30 μmol/kg) was immediate or delayed, systemic or local and combined or not with wound resection. Actinide urinary and tissue levels were measured. RESULTS: Comparison of Pu nitrate and MOX dissemination at the wound site indicated a more heterogeneous localization of MOX particles. In all cases DTPA treatment reduced target tissue (bone, liver) activity levels even if DTPA treatment was started 7 days after contamination. Surgery alone increased urinary excretion suggesting release from the wound site but no subsequent increases in organ retention (bone, liver) were observed. The combination of surgery and DTPA increased Pu excretion and reduced tissue levels markedly. CONCLUSION: This rodent model of actinide wound contamination has been used to test different treatments. It provides evidence of activity release as a result of surgery that seems not to lead to increased organ retention.
BACKGROUND: Treatment of actinide-contaminated wounds may be problematic because of contaminant physicochemical properties, dissemination and anatomical localization. This study investigates different chelation/resection protocols after contamination of rats with americium (Am) or plutonium (Pu) nitrate or mixed oxide (MOX; uranium (U), Pu oxide). METHODS: Anesthetized rats were contaminated with Am or Pu nitrate (moderately soluble) or MOX (insoluble) following wounding of hind leg muscle. DTPA (diethylene triamine pentaacetic acid) treatment (30 μmol/kg) was immediate or delayed, systemic or local and combined or not with wound resection. Actinide urinary and tissue levels were measured. RESULTS: Comparison of Pu nitrate and MOX dissemination at the wound site indicated a more heterogeneous localization of MOX particles. In all cases DTPA treatment reduced target tissue (bone, liver) activity levels even if DTPA treatment was started 7 days after contamination. Surgery alone increased urinary excretion suggesting release from the wound site but no subsequent increases in organ retention (bone, liver) were observed. The combination of surgery and DTPA increased Pu excretion and reduced tissue levels markedly. CONCLUSION: This rodent model of actinide wound contamination has been used to test different treatments. It provides evidence of activity release as a result of surgery that seems not to lead to increased organ retention.