Study of daunorubicin cardiotoxicity prevention with pyridoxal isonicotinoyl hydrazone in rabbits

2005 ◽  
Vol 51 (3) ◽  
pp. 223-231 ◽  
Author(s):  
T. Šimůnek ◽  
I. Klimtová ◽  
J. Kaplanová ◽  
M. Štěrba ◽  
Y. Mazurová ◽  
...  
Keyword(s):  
Pyridoxal Isonicotinoyl Hydrazone

scholarly journals The Isoniazid Metabolites Hydrazine and Pyridoxal Isonicotinoyl Hydrazone Modulate Heme Biosynthesis

2018 ◽  
Vol 168 (1) ◽  
pp. 209-224 ◽  
Author(s):  
Christopher Trent Brewer ◽  
Lei Yang ◽  
Anne Edwards ◽  
Yan Lu ◽  
Jonathan Low ◽  
...  
Keyword(s):  
Heme Biosynthesis ◽  
Pyridoxal Isonicotinoyl Hydrazone

HPLC study on stability of pyridoxal isonicotinoyl hydrazone

2006 ◽  
Vol 40 (1) ◽  
pp. 105-112 ◽  
Author(s):  
P. Kovaříková ◽  
M. Mokrý ◽  
J. Klimeš ◽  
K. Vávrová
Keyword(s):  
Pyridoxal Isonicotinoyl Hydrazone ◽  
Hplc Study

Pyridoxal isonicotinoyl hydrazone inhibition of FXR is involved in the pathogenesis of isoniazid-induced liver injury

2020 ◽  
Vol 402 ◽  
pp. 115134
Author(s):  
Guoqiang Zhang ◽  
Lin Chen ◽  
Yuanjie Wen ◽  
Zhi Rao ◽  
Yuhui Wei ◽  
...  
Keyword(s):  
Liver Injury ◽  
Pyridoxal Isonicotinoyl Hydrazone

IR Studies of Iron Complexes with Pyridoxal Isonicotinoyl Hydrazone and Three Other Similar Chelating Agents

1993 ◽  
Vol 26 (6) ◽  
pp. 1065-1072 ◽  
Author(s):  
C. Colonna ◽  
A. Cossé-Barbi ◽  
A. Massat ◽  
J. P. Doucet
Keyword(s):  
Chelating Agents ◽  
Iron Complexes ◽  
Ir Studies ◽  
Pyridoxal Isonicotinoyl Hydrazone

The Potential of Iron Chelators of the Pyridoxal Isonicotinoyl Hydrazone Class as Effective Antiproliferative Agents III: The Effect of the Ligands on Molecular Targets Involved in Proliferation

Blood ◽  
1999 ◽  
Vol 94 (2) ◽  
pp. 781-792 ◽  
Author(s):  
G. Darnell ◽  
D.R. Richardson
Keyword(s):  
Cell Cycle ◽  
Cell Lines ◽  
Rna Binding ◽  
Neuroblastoma Cells ◽  
Molecular Targets ◽  
Binding Activity ◽  
Time Dependent ◽  
Mrna Levels ◽  
Iron Regulatory Proteins ◽  
Pyridoxal Isonicotinoyl Hydrazone

We have identified specific iron (Fe) chelators of the pyridoxal isonicotinoyl hydrazone (PIH) class that are far more effective ligands than desferrioxamine (DFO; Richardson et al, Blood 86:4295, 1995; Richardson and Milnes, Blood 89:3025, 1997). In the present study, we have compared the effect of DFO and one of the most active chelators (2-hydroxy-1-naphthylaldehyde isonicotinoyl hydrazone; 311) on molecular targets involved in proliferation. This was performed to further understand the mechanisms involved in the antitumor activity of Fe chelators. Ligand 311 was far more active than DFO at increasing Fe release from SK-N-MC neuroepithelioma and BE-2 neuroblastoma cells and preventing Fe uptake from transferrin. Like DFO, 311 increased the RNA-binding activity of the iron-regulatory proteins (IRPs). However, despite the far greater Fe chelation efficacy of 311 compared with DFO, a similar increase in IRP-RNA binding activity occurred after 2 to 4 hours of incubation with either chelator, and the binding activity was not inhibited by cycloheximide. These results suggest that, irrespective of the Fe chelation efficacy of a ligand, an increase IRP-RNA binding activity occurred via a time-dependent step that did not require protein synthesis. Further studies examined the effect of 311 and DFO on the expression of p53-transactivated genes that are crucial for cell cycle control and DNA repair, namely WAF1,GADD45, and mdm-2. Incubation of 3 different cell lines with DFO or 311 caused a pronounced concentration- and time-dependent increase in the expression of WAF1 and GADD45 mRNA, but not mdm-2 mRNA. In accordance with the distinct differences in Fe chelation efficacy and antiproliferative activity of DFO and 311, much higher concentrations of DFO (150 μmol/L) than 311 (2.5 to 5 μmol/L) were required to markedly increase GADD45 and WAF1 mRNA levels. The increase in GADD45 and WAF1 mRNA expression was seen only after 20 hours of incubation with the chelators and was reversible after removal of the ligands. In contrast to the chelators, the Fe(III) complexes of DFO and 311 had no effect on increasing GADD45 and WAF1 mRNA levels, suggesting that Fe chelation was required. Finally, the increase in GADD45 and WAF1 mRNAs appeared to occur by a p53-independent pathway in SK-N-MC and K562 cells, because these cell lines lack functional p53. Our results suggest that GADD45 and WAF1 may play important roles in the cell cycle arrest observed after exposure to these chelators.

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