Selenite induction of DNA strand breaks and apoptosis in mouse leukemic L1210 cells

Junxuan Lu, Mark Kaeck, Cheng Jiang, Adrian C. Wilson, Henry J. Thompson

Research output: Contribution to journalArticle

129 Scopus citations

Abstract

The effects of selenite on DNA integrity, cell viability, and long-term proliferative potential of mouse leukemic L1210 cells were examined in this study. Selenite treatment resulted in concentration-dependent increases in DNA single-strand breaks and double-strand breaks, as detected by a modified filter elution assay. A time-course experiment showed that DNA single-strand breaks preceded DNA double-strand breaks. Agarose gel electrophoresis of DNA extracted from selenite-treated cells displayed a nucleosomal fragmentation pattern that is characteristics of apoptotic cell death. The involvement of a Ca2+, Mg2+-dependent endonuclease responsible for DNA double-strand fragmentation was implied by the observation that two inhibitors of endonuclease activity, i.e. aurintricarboxylic acid and zinc, blocked selenite-induced DNA double-strand breaks. These inhibitors also prevented selenite-induced cell death as defined by loss of ability to exclude trypan blue dye. Selenite treatment severely impaired the colony-forming ability of cell capable of trypan blue exclusion. The induction of DNA strand breaks and commitment to apoptosis may explain the selenite-mediated growth inhibition and loss of long-term proliferative potential.

Original languageEnglish (US)
Pages (from-to)1531-1535
Number of pages5
JournalBiochemical Pharmacology
Volume47
Issue number9
DOIs
StatePublished - Apr 29 1994

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Pharmacology

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