Alkohol wurde chronisch an weibliche Sprague Dawley-Ratten in einer ernährungsbedingten, absolut flüssigen Diät für 28 Tage verabreicht. Dies führte zu hepatischer Steatose und Lipidperoxidation. Taurin, bei gleichzeitiger Verabreichung mit Alkohol, reduzierte die hepatische Steatose und verhinderte die Lipidperoxidation vollständig.
Die schützenden Eigenschaften von Taurin bei der Verhinderung von Fettleber wurden auch histologisch nachgewiesen. Obwohl Alkohol gefunden wurde, um die Harnausscheidung von Taurin nicht zu beeinträchtigen (ein nicht-invasiver Marker der Leberschädigung), wurden die Serum- und Lebertorin-Werte bei Tieren, die Alkoholtaurin erhielten, deutlich erhöht, im Vergleich zu Tieren, die Taurin allein gegeben wurden. Die Ethanol-induzierbare Form von Cytochrom P-450 (CYP2E1) wurde durch Alkohol signifikant induziert; die Aktivität war signifikant niedriger als die Kontrollen und kaum nachweisbar bei Tieren, die die flüssige Alkohol-Diät mit Taurin gefüttert wurden.
Zusätzlich erhöhte Alkohol die Homocysteinausscheidung während der 28-tägigen Ethanol-Verabreichung in den Urin. Taurin hat diesen Anstieg jedoch nicht verhindert. Es gab Hinweise auf eine leichte Cholestase bei Tieren, die mit Alkohol und Alkoholtaurin behandelt wurden, wie durch erhöhte Serum-Gallensäuren und alkalische Phosphatase (ALP) angedeutet. Die schützenden Wirkungen von Taurin wurden dem Potenzial von Gallensäuren, insbesondere Taurin-konjugierten Gallensäuren (Taurocholsäure) zugeschrieben, um die Aktivität einiger mikrosomaler Enzyme (CYP2E1) zu hemmen. Diese vivo-Befunde zeigen zum ersten Mal, dass hepatische Steatose und Lipidperoxidation, die durch chronischen Alkoholkonsum auftreten, durch Verabreichung von Taurin an Ratten verbessert werden können.
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