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Chapter 6 - Cellular copper toxicity: A critical appraisal of fenton-chemistry based oxidative stress in Wilson disease.
In: Wilson Disease; Pathogenesis, Molecular Mechanisms, Diagnosis, Treatment and Monitoring. 2019. 65-81
The redox activity of copper is of vital importance for biochemical and
bioenergetic cellular homeostasis. However, cellular copper overload
leads to cell death. Wilson disease patients suffer from such toxic
copper overload, especially in their livers. It has been suggested that
this accumulating liver copper may catalyze the formation of highly
detrimental hydroxyl radicals. However, diverse findings, like the lack
of free copper in cells, have challenged such a Fenton-chemistry-based
copper toxicity. To weigh these uncertainties, we provide here a survey
of studies on oxidative stress markers in WD patients and related animal
models and on therapies that aimed at avoiding oxidative stress in WD
animals. Collectively, these reports demonstrate that a
Fenton-chemistry-based copper toxicity is a concurrent feature with
clinically apparent hepatitis in WD animals. However, such oxidative
damage is hardly detectable in earlier disease stages, and antioxidative
therapies do delay but do not avoid hepatitis. Thus, a
Fenton-chemistry-based copper toxicity may be regarded as a major
executioner of hepatocyte damage or death, but it does not appear to be
the driving toxic mechanism leading to this disease stage.
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Publikationstyp
Artikel: Sammelbandbeitrag/Buchkapitel
Schlagwörter
Oxidative stress;
Fenton chemistry;
Copper;
Wilson disease;
Liver;
Copper chelator
Bandtitel
Wilson Disease; Pathogenesis, Molecular Mechanisms, Diagnosis, Treatment and Monitoring
Quellenangaben
Seiten: 65-81
Nichtpatentliteratur
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