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.

Biochemical grounds for "crosslinker sensitivity": What have we learned from pharmacology?

D'ISCHIA, MARCO;
2015

Abstract

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.
2015
Fanconi Anemia and Oxidative Stress: Mechanistic Background and Clinical Prospects
Nova Science Publishers, Inc.
Bioactivation; Diepoxybutane; Mitomycin c; Redox mechanisms; Medicine (all)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11384/83853
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