Selenomethionine or methylseleninic acid inhibits mutagenesis of a reporter gene in mouse bone marrow

Ma Suresh Kumar, Karen E. Pollok, Martin L. Smith

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Recent laboratory and clinical studies have utilized selenium in the form of pure seleno-L-methionine (SeMet) in combination with DNA-damaging cancer chemotherapy drugs. In mice, the selenium protected bone marrow and other tissues from dose-limiting toxicity. In fact, because of the protection from dose-limiting toxicity, a doubling or even tripling of the maximum tolerated dose (MTD) was enabled. Previously we showed that SeMet protects bone marrow by a DNA repair mechanism that requires the XPC DNA repair protein. XPC is rate-limiting and is required for repair of cisplatin or carboplatin adducts. Herein we used a mouse strain that carries a lambda phage reporter gene in the genome that serves as a mutagenesis target. SeMet protects from carboplatin mutagenesis in mouse bone marrow. Methylseleninic acid (MSA), a metabolite of SeMet, also protected against mutagenesis in mouse bone marrow.

Original languageEnglish (US)
Pages (from-to)291-293
Number of pages3
JournalAnticancer Research
Volume30
Issue number2
StatePublished - Feb 1 2010

Keywords

  • Carboplatin
  • Cisplatin
  • DNA repair
  • Nucleotide excision repair
  • Selenium

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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