Zusammenfassung
Viele Erkrankungen werden mit einem oxidativen Schaden durch Sauerstoffradikale in
Verbindung gebracht, wobei solche Schäden durch das Ungleichgewicht zwischen dem Radikalbildungssystem
und dem Radikalabbausystem entstehen. Dieser Zustand wird als oxidativer Stress bezeichnet.
Bei Patienten mit Hepatitis oder anderen chronischen Lebererkrankungen wurde ein erhöhter
oxidativer Stress nachgewiesen. Experimentelle Studien haben auch den Zusammenhang
zwischen der Überproduktion von Sauerstoffradikalen in der Reperfusionsphase und einen
darauf folgenden Gewebsschaden nach Lebertransplantation festgestellt. Nahezu alle
Zelltypen in der Leber haben die Fähigkeit freie Sauerstoffradikale zu bilden; diese
sind als auslösende und modulierende Faktoren an der Entstehung und Progression von
Lebererkrankungen beteiligt. Glutathion, ein in der Leber synthetisiertes Tripeptid,
spielt eine wesentliche Rolle bei der Verhinderung von oxidativem Stress. Ein Mangel
an Glutathion bzw. anderen Antioxidantien in der Leber verstärkt die weitere Progression
von Leberzellschäden und wurde bei unterschiedlichen Lebererkrankungen festgestellt.
Die Hemmung der Produktion von Sauerstoffradikalen durch Antioxidantien ist ein logischer
Ansatz bei der Behandlung von Leberzellschäden. Vitamin C, E, A und β-Karotin sind
effektive Radikalfänger von Sauerstoff. In den letzten Jahren wurden einige neue Methoden
entwickelt, wobei diese auf der Genübertragung antioxidativer Enzyme beruhen. Die
Messung von oxidativen Schäden kann durch spezifische Biomarker quantifiziert werden.
Experimentelle Daten zu diesem Thema konnten jedoch klinisch nicht verifiziert werden.
Zum kausalen Zusammenhang zwischen dem Ausmaß des oxidativen Stresses bzw. den oxidativen
Stressparametern einerseits und dem klinischen Verlauf beim Patienten andererseits,
gibt es sehr wenige Daten. Zur Standardisierung der antioxidativen Behandlung und
zur besseren Beobachtung der Progression von Lebererkrankungen bei dieser Behandlung
sind weitere Studien notwendig.
Abstract
Many diseases are linked to oxidative damage from reactive oxygen species as a result
of an imbalance between radical generating and radical scavenging systems, a condition
known as oxidative stress. In patients with hepatitis or other chronic liver diseases,
there is consistent evidence of enhanced oxidative stress. Experimental studies have
also elucidated the relationship between the hyperproduction of reactive oxygen species
during the reperfusion phase and ischemia-reperfusion tissue injury. Nearly all cell
types in the liver have the capacity to generate oxygen-free radicals, which participate
as initiating factors and modulators in the induction and progression of liver disease.
Glutathione, a tripeptide synthetised in the liver, plays a crucial role against oxidative
stress. A deficiency of hepatic glutathione and its antioxidant partners are found
to be reduced in liver diseases, which amplifies further progression of liver cell
damage. Inhibition of reactive oxygen species production and augmentation of antioxidant
defences is a logical approach in the treatment of liver cell damage. Vitamins C,
E, A and β carotene are found to be effective as scavengers of reactive oxygen species.
Some new approaches based on gene delivery of antioxidant enzymes have been developed.
The measurement of oxidative damage can be quantified by the specific biomarkers of
altered redox state. However, experimental data on this subject have not always been
confirmed clinically. Very few data are available on the causal relationship between
the degree of oxidative damage or oxidative stress parameters and the outcome of patients.
Future research is required to standardise the antioxidative treatment and to better
observe the progression of liver diseases during this treatment.
Schlüsselwörter
Oxidativer Stress - Sauerstoffradikale - Lebererkrankung - Antioxidantien - oxidative
Stressparameter
Key words
Oxidative stress - reactive oxygen species - liver disease - antioxidants - oxidative
stress parameters
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Dr. Heinz Steltzer
Department of Anesthesiology und General Intensive Care · Vienna General Hospital
· University of Vienna
Waehringer Guertel 18 - 20
1090 Vienna · Austria, Europe
eMail: heinz.steltzer@akh-wien.ac.at
