Abstract
Within minutes of exposure of target cells to cytotoxic T lymphocytes, their nuclear DNA begins to be fragmented. This phenomenon precedes 51Cr release by at least an hour. DNA fragmentation occurs only when appropriately sensitized cytotoxic T cells are used and is not merely a result of cell death because killing of target cells by heating, freeze/thawing, or lysing with antibody and complement did not yield DNA fragments. Agarose gel electrophoresis of target cell DNA showed discrete multiples of an approximately 200-base-pair subunit, suggesting that fragmentation was the result of activation of a specific endonuclease. A similar pattern of DNA fragments is observed during glucocorticoid-induced killing of mouse thymocytes. The endonuclease in that case is inhibited by zinc ions, and we find that Zn2+ also inhibits DNA fragmentation and 51Cr release induced by cytotoxic T cells, suggesting a final common biochemical pathway for both types of cell death.
Keywords
Cytotoxic T cellEndonucleaseMolecular biologyFragmentation (computing)DNABiologyCytolysisDNA fragmentationLysisAgarose gel electrophoresisDNA damageProgrammed cell deathBiochemistryIn vitroApoptosis
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Publication Info
- Year
- 1983
- Type
- article
- Volume
- 80
- Issue
- 20
- Pages
- 6361-6365
- Citations
- 616
- Access
- Closed
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Cite This
Richard C. Duke,
Robert Chervenak,
John Cohen
(1983).
Endogenous endonuclease-induced DNA fragmentation: an early event in cell-mediated cytolysis..
Proceedings of the National Academy of Sciences
, 80
(20)
, 6361-6365.
https://doi.org/10.1073/pnas.80.20.6361
Identifiers
- DOI
- 10.1073/pnas.80.20.6361