The literature pointing to mitomycin C bioactivation, and to the toxicity mechanisms of diepoxybutane and a group of nitrogen mustards causing DNA crosslinks in Fanconi Anemia (FA) cells is reviewed. A critical analysis of this literature prompts revisiting the FA phenotype and crosslinker sensitivity in terms of an oxidative stress (OS) background, redox-related anomalies of FA (FANC) proteins, and mitochondrial dysfunction. This re-appraisal of FA basic defect might lead to innovative approaches both in elucidating FA phenotype and in prospect developments of patients' clinical management.
|Titolo:||Biochemical grounds for "crosslinker sensitivity": What have we learned from pharmacology?|
|Titolo del libro:||Fanconi Anemia and Oxidative Stress: Mechanistic Background and Clinical Prospects|
|Editore:||Nova Science Publishers, Inc.|
|Data di pubblicazione:||2015|
|Parole Chiave:||Bioactivation; Diepoxybutane; Mitomycin c; Redox mechanisms; Medicine (all)|
|Appare nelle tipologie:||2.1 Contributo in volume (Capitolo o Saggio)|