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Selective increase of dATP pools upon activation of deoxycytidine kinase in lymphocytes: implications in apoptosis

Gergely Keszler1, Tatjana Spasokoukotskaja, Zsolt Csapo

  • 1Institute of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.

Nucleosides, Nucleotides & Nucleic Acids
|December 2, 2004
PubMed

Insights

Deoxycytidine kinase (dCK) activation may promote apoptosis by increasing dATP levels, crucial for cell death signaling. This enzyme

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Deoxycytidine kinase (dCK) is a key enzyme in deoxynucleoside salvage.
  • dCK stimulation is linked to cellular responses against DNA damage and apoptosis.
  • The role of dCK activation in apoptosis induction warrants investigation.

Purpose of the Study:

  • To investigate the role of deoxycytidine kinase (dCK) activation in apoptosis.
  • To determine if dCK activation contributes to apoptosis by modulating deoxynucleotide triphosphate (dNTP) pools.
  • To explore the potential of dCK as a pro-apoptotic factor.

Main Methods:

  • Human tonsillar lymphocytes were exposed to 2-chloro-deoxyadenosine (CdA).
  • dCK activity was measured following CdA treatment.
  • The effect of pifithrin-alpha, a p53 inhibitor, on dCK activation was assessed.
  • Deoxynucleotide triphosphate (dNTP) pools were quantified using specific assays.

Main Results:

  • Exposure to CdA resulted in a two-fold increase in dCK activity.
  • Pifithrin-alpha inhibited CdA-induced dCK activation, suggesting p53 involvement.
  • CdA, aphidicolin, and etoposide treatments led to increased dATP levels.
  • Deoxypyrimidine triphosphate and dGTP pools were reduced post-treatment.

Conclusions:

  • dCK activation, induced by cellular damage, may act as a pro-apoptotic factor.
  • This activation generates elevated dATP levels, potentially preceding mitochondrial damage.
  • dCK's role in supplying dATP for apoptosome formation is a key finding.

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