These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Selenomethionine or methylseleninic acid inhibits mutagenesis of a reporter gene in mouse bone marrow.
    Author: Kumar MS, Pollok KE, Smith ML.
    Journal: Anticancer Res; 2010 Feb; 30(2):291-3. PubMed ID: 20332431.
    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.
    [Abstract] [Full Text] [Related] [New Search]