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Spermine prevents cytochrome c release in glucocorticoid-induced apoptosis in mouse thymocytes.

  • Cecilia Hegardt
  • Gunnar Andersson
  • Stina Oredsson
Publishing year: 2003
Language: English
Pages: 115-121
Publication/Series: Cell Biology International
Volume: 27
Issue: 2
Document type: Journal article
Publisher: Elsevier

Abstract english

Apoptosis can be induced in primary cultures of mouse thymocytes using the glucocorticoid dexamethasone. Addition of the polyamine spermine simultaneously with dexamethasone reduces the induction of apoptosis compared to treatment with dexamethasone alone. We investigated the signal transduction pathway at the mitochondrial level in order to elucidate spermine's protective effect. Mitochondrial involvement is evident due to the loss of mitochondrial transmembrane potential, release of cytochrome c into the cytosol and activation of caspase-9 in dexamethasone-treated thymocytes. The addition of spermine inhibited the release of cytochrome c from the mitochondria into the cytosol, and also the activation of caspase-9. When the mitogen concanavalin A (Con A) was added to dexamethasone- plus spermine-treated thymocytes, the number of apoptotic cells in the pre-G1peak was reduced compared to thymocytes treated with only dexamethasone plus spermine. Comparing concanavalin A added to dexamethasone-treated or to dexamethasone plus spermine-treated thymocytes, showed a markedly reduced pre-G1peak in the latter. Thus, the spermine-induced inhibition of cytochrome c release confers a survival advantage on thymocytes.


  • Zoology


  • ISSN: 1095-8355
Stina Oredsson
E-mail: stina [dot] oredsson [at] biol [dot] lu [dot] se


Functional zoology

+46 46 222 94 97



Principal investigator

LUCC - Lund University Cancer Centre

Research group

Animal Physiology


Cell proliferation

Doctoral students and postdocs

PhD Students, main supervisor

Wendy Soria Sotillo

PhD Students, assistant supervisor

Atena Malakpour Permlid