Redox state defects in fanconi's anemia

P. Degan Miaoi, O. A. Zunino, S. Borghini, A. Abbondandolo

Research output: Contribution to journalArticlepeer-review

Abstract

Biochemical steps toward the deregulation from a physiological and healthy to a pathological situation seems to share as a common denominator the ability to us, tile modulation of tile redox stale of the cells as a general regulatory pathway from t he embryonic development to mature tissue. The quantification of S-OttdG in I)NA extracted from cells and tissues, is used as reference to measure the oxidative stress. The lesson that we are learning from tile study of Tile behaviour of cells and tissues experiencing enhanced oxidative stress because of environmental exposure to toxic or mutagenic substances or genetic and metaboli(: susceptibility is that the high oxidative stress tags cells that are meanl to undergo degenerative or cancerogenic processes. The most complex and challenging situation is the one that we see in some genetic diseases ( such as l"allc(mi's anemia, Ataxia Telangienctasia, Bloom and Down syndromes) lhat have common characteristic of a premature ageing process and are yet prone to carcinogenic processes, tlere an abnormal metabolism of the oxygen is found and also abnormal mitochondrial functioning is reported whenever specific studies arc performed. We feel that in order to better understand the phenotypic abnormalities in these complex pathologies we need to study the relationships between lhe detects of the redox state at the citoplasmic, nu(lear and mitochondrial level. To (late we are focusing our experience on t h, Fan('oni's anemia.

Original languageEnglish
JournalFASEB Journal
Volume11
Issue number9
Publication statusPublished - Dec 1 1997

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Fingerprint Dive into the research topics of 'Redox state defects in fanconi's anemia'. Together they form a unique fingerprint.

Cite this