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Amifostine induces antioxidant enzymatic activities in normal tissues and a transplantable tumor that can affect

David J Grdina1, Jeffrey S Murley, Yasushi Kataoka

  • 1Department of Radiation and Cellular Oncology, The University of Chicago, Chicago, IL 60637, USA. dgrdina@uchicago.edu

International Journal of Radiation Oncology, Biology, Physics
|February 14, 2009
PubMed
Abstract

Insights

Amifostine treatment increases manganese superoxide dismutase (SOD2) in mouse tissues and tumors, offering delayed radioprotection. However, elevated SOD2 in tumors may reduce radiation therapy effectiveness.

Area of Science:

  • Biochemistry
  • Oncology
  • Radiology

Background:

  • Amifostine is a radioprotective agent.
  • Manganese superoxide dismutase (SOD2) is a key antioxidant enzyme.
  • Understanding amifostine's impact on SOD2 is crucial for optimizing cancer treatment.

Purpose of the Study:

  • To investigate if amifostine induces elevated SOD2 in murine tissues and SA-NH tumors.
  • To determine if this elevation results in a delayed radioprotective effect on tumor cells.

Main Methods:

  • SA-NH tumor-bearing mice received amifostine via intraperitoneal injection (single or fractionated doses).
  • Enzymatic activity of SOD2, catalase, and glutathione peroxidase (GPx) was measured in various tissues and tumors.
  • The impact of elevated SOD2 on SA-NH cell radiation response was assessed.

Main Results:

  • Amifostine significantly elevated SOD2 activity in tissues and tumors 24 hours post-treatment.
  • SA-NH tumor cells showed a twofold increase in SOD2 activity and a 27% increase in radiation resistance.
  • Fractionated amifostine doses also increased antioxidant enzyme levels.

Conclusions:

  • Amifostine induces a delayed radioprotective effect linked to elevated SOD2 in SA-NH tumors.
  • Elevated SOD2 in normal tissues may enhance overall radiation protection.
  • Elevated tumor SOD2 could potentially reduce the efficacy of fractionated radiation therapy.

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