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Related Experiment Videos

Is Ap4A involved in DNA repair processes?

G Gilson1, J P Ebel, P Remy

  • 1Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.

Experimental Cell Research
|July 1, 1988
PubMed
Summary

N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) exposure causes a significant accumulation of bisnucleosides polyphosphates (Ap4X) in cells, especially when ADP-ribosyltransferase (ADPRT) is inhibited. This response differs from heat shock effects.

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Area of Science:

  • Cellular biology
  • Biochemistry
  • Molecular toxicology

Background:

  • Bisnucleosides polyphosphates (Ap4X) are signaling molecules with roles in cellular stress responses.
  • ADP-ribosyltransferase (ADPRT) is an enzyme involved in DNA repair and other cellular processes.

Purpose of the Study:

  • To investigate the effect of the alkylating agent N-methyl-N itro-N-nitrosoguanidine (MNNG) on Ap4X pool size in hepatoma tissue culture (HTC) cells.
  • To compare the cellular response to MNNG with that of heat shock regarding Ap4X accumulation and ADPRT activity.

Main Methods:

  • Hepatoma tissue culture (HTC) cells were treated with MNNG, 3-aminobenzamide (3AB), or heat shock.
  • Ap4X pool size and ADP-ribosyltransferase (ADPRT) activity were measured.
  • Protein synthesis inhibition was also assessed.

Main Results:

  • MNNG treatment induced a transient accumulation of Ap4X, which was enhanced and prolonged by 3AB, an ADPRT inhibitor.
  • Heat shock caused a different pattern of Ap4X accumulation, unaffected by 3AB.
  • Both MNNG and heat shock inhibited protein synthesis, but MNNG enhanced ADPRT activity while heat shock had minimal effect.

Conclusions:

  • MNNG-induced Ap4X accumulation in eukaryotic cells is distinct from heat shock-induced accumulation.
  • Ap4X compounds are likely involved in DNA excision repair, a process implicated with the ADPRT enzyme.

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