TY - JOUR
T1 - Cytotoxic evaluation of 3-aminopyridine-2-carboxaldehyde thiosemicarbazone in peripheral blood lymphocytes of patients with refractory solid tumors using electron paramagnetic resonance
AU - Kolesar, Jill M.
AU - Sachidanandam, Kamakshi
AU - Schelman, William R.
AU - Eickhoff, Jens
AU - Holen, Kyle D.
AU - Traynor, Anne M.
AU - Alberti, Dona B.
AU - Thomas, James P.
AU - Chitambar, Christopher R.
AU - Wilding, George
AU - Antholine, William E.
PY - 2011/1
Y1 - 2011/1
N2 - 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone (3-APAP) is a metal chelator that potently inhibits the enzyme ribonucleotide reductase (RRRR), which plays a key role in cell division and tumor progression. A subunit of RRRR has a non-heme iron and a tyrosine-free radical, which are required for the enzymatic reduction of ribonucleotides to deoxyribonucleotides. The objective of the present study was to determine whether 3-APAP affects its targeted action by measuring electron paramagnetic resonance (EPRPR) signals formed either directly or indirectly from low molecular weight ferric-3-APAP chelates. Peripheral blood lymphocytes were collected from patients with refractory solid tumors at baseline and at 2, 4.5 and 22h after 3-APAP administration. Using EPRPR spectra, our study identified signals from high-spin Fe-transferrin, high-spin heme and low-spin iron or copper ions. An increase in the Fe-transferrin signal was observed, suggesting blockage of Fe uptake. It is hypothesized that formation of reactive oxygen species by FeT2 or CuT damages the transferrin or the transferrin receptor. An increase in the heme signal was also observed, which was a probable source of cytochromec release from the mitochondria and potential apoptosis. In addition, increased levels of Fe and Cu were identified. These results, which were consistent with our previous study validating 3-AP-mediated signals by EPR, provide valuable insights into the in vivo mechanism of action of 3-AP.
AB - 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone (3-APAP) is a metal chelator that potently inhibits the enzyme ribonucleotide reductase (RRRR), which plays a key role in cell division and tumor progression. A subunit of RRRR has a non-heme iron and a tyrosine-free radical, which are required for the enzymatic reduction of ribonucleotides to deoxyribonucleotides. The objective of the present study was to determine whether 3-APAP affects its targeted action by measuring electron paramagnetic resonance (EPRPR) signals formed either directly or indirectly from low molecular weight ferric-3-APAP chelates. Peripheral blood lymphocytes were collected from patients with refractory solid tumors at baseline and at 2, 4.5 and 22h after 3-APAP administration. Using EPRPR spectra, our study identified signals from high-spin Fe-transferrin, high-spin heme and low-spin iron or copper ions. An increase in the Fe-transferrin signal was observed, suggesting blockage of Fe uptake. It is hypothesized that formation of reactive oxygen species by FeT2 or CuT damages the transferrin or the transferrin receptor. An increase in the heme signal was also observed, which was a probable source of cytochromec release from the mitochondria and potential apoptosis. In addition, increased levels of Fe and Cu were identified. These results, which were consistent with our previous study validating 3-AP-mediated signals by EPR, provide valuable insights into the in vivo mechanism of action of 3-AP.
KW - 3-aminopyridine-2-carboxaldehyde thiosemicarbazone
KW - Chelator
KW - Electron paramagnetic resonance
KW - Ribonucleotide reductase
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U2 - 10.3892/etm.2010.165
DO - 10.3892/etm.2010.165
M3 - Article
AN - SCOPUS:78751615964
SN - 1792-0981
VL - 2
SP - 119
EP - 123
JO - Experimental and Therapeutic Medicine
JF - Experimental and Therapeutic Medicine
IS - 1
ER -