Taurine Prevents Tamoxifen‐Induced Mitochondrial Oxidative Damage in Mice

:  Tamoxifen is a selective oestrogen receptor modulator widely used in the treatment of breast cancer. Tamoxifen potentially affects mitochondrial functions as it acts as an uncoupling agent and a powerful inhibitor of mitochondrial electron transport chain. There is concern for the deleterious eff...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Basic & clinical pharmacology & toxicology 2008-04, Vol.102 (4), p.382-387
Hauptverfasser: Parvez, Suhel, Tabassum, Heena, Banerjee, Basu Dev, Raisuddin, Sheikh
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung::  Tamoxifen is a selective oestrogen receptor modulator widely used in the treatment of breast cancer. Tamoxifen potentially affects mitochondrial functions as it acts as an uncoupling agent and a powerful inhibitor of mitochondrial electron transport chain. There is concern for the deleterious effects of tamoxifen. Taurine is known to have membrane stabilizing and antioxidant properties. We studied effect of taurine pre‐treatment on the toxicity of tamoxifen in mouse liver mitochondria focusing specifically on the redox cycle biomarkers. Tamoxifen caused a significant rise in the mitochondrial lipid peroxidation, protein carbonyl content and superoxide radical generation. There was a significant change in the mitochondrial thiol profile in the tamoxifen‐treated animals. Pre‐treatment of mice with taurine (100 mg/kg) markedly lowered mitochondrial lipid peroxidation, protein carbonyl content and superoxide radical generation. It also restored decreased enzymatic and non‐enzymatic antioxidants of mitochondria. It is suggested that taurine has a potential role in ameliorating tamoxifen‐induced mitochondrial toxicity, and the protection is afforded either by reversing the decline of antioxidants or by the direct free radical‐scavenging activity.
ISSN:1742-7835
1742-7843
DOI:10.1111/j.1742-7843.2008.00208.x