cytochrome-c-t and 3-aminopyridine-2-carboxaldehyde-thiosemicarbazone

cytochrome-c-t has been researched along with 3-aminopyridine-2-carboxaldehyde-thiosemicarbazone* in 2 studies

Other Studies

2 other study(ies) available for cytochrome-c-t and 3-aminopyridine-2-carboxaldehyde-thiosemicarbazone

Article	Year
Electron paramagnetic resonance study of peripheral blood mononuclear cells from patients with refractory solid tumors treated with Triapine. Journal of inorganic biochemistry, 2008, Volume: 102, Issue:4 The metal chelator Triapine, 3-aminopyridine-2-carboxaldehyde thiosemicarbazone, is a potent inhibitor of ribonucleotide reductase. EPR spectra consistent with signals from Fe-transferrin, heme, and low-spin iron or cupric ion were observed in peripheral blood mononuclear cells (PBMCs) obtained from patients treated with Triapine. One signal that is unequivocally identified is the signal for Fe-transferrin. It is hypothesized that Fe uptake is blocked by reactive oxygen species generated by FeT(2) or CuT that damage transferrin or transferrin receptor. A potential source for the increase in the heme signal is cytochrome c released from the mitochondria. These results provide valuable insight into the in vivo mechanism of action of Triapine. Topics: Cytochromes c; Electron Spin Resonance Spectroscopy; Humans; Monocytes; Neoplasms; Pyridines; Thiosemicarbazones	2008
PAN-811 (3-aminopyridine-2-carboxaldehyde thiosemicarbazone), a novel neuroprotectant, elicits its function in primary neuronal cultures by up-regulating Bcl-2 expression. Neuroscience, 2005, Volume: 135, Issue:1 Neurotoxicity in primary neurons was induced using hypoxia/hypoglycemia (H/H), veratridine (10microM), staurosporine (1microM) or glutamate (100microM), which resulted in 72%, 67%, 75% and 66% neuronal injury, respectively. 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone (PAN-811; 10microM; Panacea Pharmaceuticals, Gaithersburg, MD) pretreatment for 24 h provided maximal neuroprotection of 89%, 42%, 47% and 89% against these toxicities, respectively. Glutamate or H/H treatment of cells increased cytosolic cytochrome c levels, which was blocked by pretreatment of cells with PAN-811. Pretreatment of neurons with PAN-811 produced a time-dependent increase in the protein level of Bcl-2, which was evident even after glutamate or H/H treatments. An up-regulation in the expression of the p53 and Bax genes was also observed following exposure to these neurotoxic insults; however, this increase was not suppressed by PAN-811 pretreatment. Functional inhibition of Bcl-2 by HA14-1 reduced the neuroprotective efficacy of PAN-811. PAN-811 treatment also abolished glutamate or H/H-mediated internucleosomal DNA fragmentation. Topics: Animals; Apoptosis; Blotting, Western; Cell Survival; Cells, Cultured; Cytochromes c; DNA Fragmentation; Excitatory Amino Acid Antagonists; Genes, bcl-2; Hypoglycemia; Hypoxia; Neurons; Neuroprotective Agents; Pyridines; Rats; Rats, Sprague-Dawley; Staurosporine; Thiosemicarbazones; Up-Regulation; Veratridine	2005

Article

Year

Electron paramagnetic resonance study of peripheral blood mononuclear cells from patients with refractory solid tumors treated with Triapine.

Journal of inorganic biochemistry, 2008, Volume: 102, Issue:4

The metal chelator Triapine, 3-aminopyridine-2-carboxaldehyde thiosemicarbazone, is a potent inhibitor of ribonucleotide reductase. EPR spectra consistent with signals from Fe-transferrin, heme, and low-spin iron or cupric ion were observed in peripheral blood mononuclear cells (PBMCs) obtained from patients treated with Triapine. One signal that is unequivocally identified is the signal for Fe-transferrin. It is hypothesized that Fe uptake is blocked by reactive oxygen species generated by FeT(2) or CuT that damage transferrin or transferrin receptor. A potential source for the increase in the heme signal is cytochrome c released from the mitochondria. These results provide valuable insight into the in vivo mechanism of action of Triapine.

Topics: Cytochromes c; Electron Spin Resonance Spectroscopy; Humans; Monocytes; Neoplasms; Pyridines; Thiosemicarbazones

2008

PAN-811 (3-aminopyridine-2-carboxaldehyde thiosemicarbazone), a novel neuroprotectant, elicits its function in primary neuronal cultures by up-regulating Bcl-2 expression.

Neuroscience, 2005, Volume: 135, Issue:1

Neurotoxicity in primary neurons was induced using hypoxia/hypoglycemia (H/H), veratridine (10microM), staurosporine (1microM) or glutamate (100microM), which resulted in 72%, 67%, 75% and 66% neuronal injury, respectively. 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone (PAN-811; 10microM; Panacea Pharmaceuticals, Gaithersburg, MD) pretreatment for 24 h provided maximal neuroprotection of 89%, 42%, 47% and 89% against these toxicities, respectively. Glutamate or H/H treatment of cells increased cytosolic cytochrome c levels, which was blocked by pretreatment of cells with PAN-811. Pretreatment of neurons with PAN-811 produced a time-dependent increase in the protein level of Bcl-2, which was evident even after glutamate or H/H treatments. An up-regulation in the expression of the p53 and Bax genes was also observed following exposure to these neurotoxic insults; however, this increase was not suppressed by PAN-811 pretreatment. Functional inhibition of Bcl-2 by HA14-1 reduced the neuroprotective efficacy of PAN-811. PAN-811 treatment also abolished glutamate or H/H-mediated internucleosomal DNA fragmentation.

Topics: Animals; Apoptosis; Blotting, Western; Cell Survival; Cells, Cultured; Cytochromes c; DNA Fragmentation; Excitatory Amino Acid Antagonists; Genes, bcl-2; Hypoglycemia; Hypoxia; Neurons; Neuroprotective Agents; Pyridines; Rats; Rats, Sprague-Dawley; Staurosporine; Thiosemicarbazones; Up-Regulation; Veratridine

2005