Ascorbic acid reduced mutagenicity at the HPRT locus in CHO cells against thermal neutron radiation

Appl Radiat Isot. 2004 Nov;61(5):929-32. doi: 10.1016/j.apradiso.2004.05.011.

Abstract

We investigated the biological effects of the long-lived radicals induced following neutron irradiation. It has been reported that radiation-induced long-lived radicals were scavenged by post-irradiation treatment of ascorbic acid (Koyama, 1998). We studied the effects of ascorbic acid acting as a long-lived radical scavenger on cell killing and mutagenicity in Chinese hamster ovary cells against thermal neutrons produced at the Kyoto University Research reactor. Ascorbic acid was added to cells 30 min after neutron irradiation and removed 150 min after irradiation. The biological end point of cell survival was measured by colony formation assay. The mutagenicity was measured by the mutant frequency in the HPRT locus. The post-irradiation treatment of ascorbic acid did not alter the cell killing effect of neutron radiation. However, the mutagenicity was decreased, especially when the cells were irradiated with boron. Our results suggested that ascorbic acid scavenged long-lived radicals effectively and caused apparent protective effects against mutagenicity of boron neutron capture therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascorbic Acid / pharmacology*
  • Boron Neutron Capture Therapy / adverse effects
  • CHO Cells
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Cricetinae
  • DNA / drug effects
  • DNA / genetics*
  • DNA / radiation effects*
  • DNA Damage
  • Fast Neutrons / adverse effects*
  • Free Radical Scavengers / pharmacology*
  • Free Radicals / metabolism
  • Free Radicals / radiation effects
  • Hypoxanthine Phosphoribosyltransferase / genetics*
  • Mutation

Substances

  • Free Radical Scavengers
  • Free Radicals
  • DNA
  • Hypoxanthine Phosphoribosyltransferase
  • Ascorbic Acid