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Published on: February 16, 2015

Sorbitol-induced apoptosis of human leukemia is mediated by caspase activation and cytochrome c release

Gabriella Marfè1, Emanuela Morgante, Carla Di Stefano

  • 1Department of Experimental Medicine and Biochemical Sciences, University of Rome "Tor Vergata", Via Montpellier 1, 00133 Rome, Italy. gabriellamarfe@libero.it

Archives of Toxicology
|November 30, 2007
PubMed

Insights

Sorbitol triggers apoptosis in K562 cancer cells by activating caspase 3 and altering Bcl-2 family proteins. This process involves mitochondrial dysfunction and cytochrome c release, offering insights into cancer cell death mechanisms.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Sorbitol is known to induce apoptosis in various cancer cell lines.
  • The precise molecular mechanisms of sorbitol-induced apoptosis remain unclear.

Purpose of the Study:

  • To investigate the intracellular signaling pathways involved in sorbitol-induced apoptosis in human K562 cells.
  • To elucidate the role of Bcl-2 family proteins, mitochondrial pathways, and caspase 3 in this process.

Main Methods:

  • Morphological analysis and DNA fragmentation assays were employed.
  • Changes in Bcl-2 family protein expression (Bax, p-Bcl-2, Bcl-X(L)) were assessed.
  • Mitochondrial membrane potential, cytochrome c release, and caspase 3 activation were measured.

Main Results:

  • Sorbitol induced apoptosis in K562 cells in a concentration- and time-dependent manner.
  • Apoptosis was associated with increased Bax, decreased p-Bcl-2, reduced mitochondrial membrane potential, and elevated cytochrome c release.
  • Caspase 3 activation was observed, and its inhibition prevented cell death.

Conclusions:

  • Sorbitol-induced apoptosis in K562 cells involves the mitochondrial pathway and caspase 3 activation.
  • Bcl-2 family proteins and mitochondrial integrity play critical roles in this apoptotic process.

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