Bile salts modulate chronic ethanol-induced hepatotoxicity.

نویسندگان

  • Anne-Marie Montet
  • Laurence Oliva
  • Françoise Beaugé
  • Jean-Claude Montet
چکیده

This study tested the hypothesis that chronic ethanol-induced injury in rats may be modified by the hydrophobicity of the bile acid pool. The supplementation to chronic ethanol feeding (28 days) with chenodeoxycholate, a hydrophobic bile salt, aggravated steatosis (accumulation of triacylglycerols and cholesterol esters), lipoperoxidation and cytolysis (expressed as elevations of activities of aspartate aminotransferase and glutamate dehydrogenase), while the addition of ursodeoxycholic acid, a hydrophilic bile salt, alleviated ethanol-induced hepatic alterations. Furthermore, our data show that ursodeoxycholic acid still exerts its beneficial effects in a model of more severe hepatic intoxication induced by the co-administration of ethanol and chenodeoxycholic acid. The hepato-protective effect observed appears to be independent of the choleretic properties of ursodeoxycholic acid and may be due partly to the capacity of the bile acid to preserve mitochondria.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Role of membrane transport in hepatotoxicity and pathogenesis of drug-induced cholestasis

Drug-induced liver injury is an important clinical entity, which can be grouped into cholestatic liver injury, hepatocellular liver injury, and mixed liver injury. Cholestatic liver injury is characterized by a reduction in bile flow and the retention within hepatocytes of cholephilic compounds such as bile salts that cause hepatotoxicity. Bile salts are taken up by hepatocytes in a largely sod...

متن کامل

Ritonavir, saquinavir, and efavirenz, but not nevirapine, inhibit bile acid transport in human and rat hepatocytes.

Human immunodeficiency virus-infected patients on antiretroviral drug therapy frequently experience hepatotoxicity, the underlying mechanism of which is poorly understood. Hepatotoxicity from other compounds such as bosentan and troglitazone has been attributed, in part, to inhibition of hepatocyte bile acid excretion. This work tested the hypothesis that antiretroviral drugs modulate hepatic b...

متن کامل

protective effect of hydro alcoholic extract of Aloysia citriodora against ethanol-induced hepatotoxicity in male Wistar rats via assessment of inflammatory and oxidative stress markers

Objective: Chronic ethanol consumption has significant negative effects on liver tissue. Mechanisms of ethanol toxicity include oxidative stress and inflammation. The antioxidant and anti-inflammatory properties of the lemon verbena have been proven in studies. The aim of this study was to evaluate the protective effect of hydro alcoholic extract of Aloysia citriodora (AC) on ethanol-induced he...

متن کامل

Protective role of licochalcone B against ethanol-induced hepatotoxicity through regulation of Erk signaling

Objective(s): Oxidative stress has been established as a key cause of alcohol-induced hepatotoxicity. Licochalcone B, an extract of licorice root, has shown antioxidative properties. This study was to investigate the effects and mechanisms of licochalcone B in ethanol-induced hepatic injury in an in vitro study. Materials and Methods: An in vitro model of Ethanol-induced cytotoxicity in BRL cel...

متن کامل

Liver toxicity of sitaxentan in pulmonary arterial hypertension.

Hepatotoxicity is a frequent side-effect of ERA therapy, which is contra-indicated in patients with mild to severe hepatic impairment (Child–Pugh class B–C) and elevated serum aminotransferases prior to initiation of treatment. In addition, liver function testing on a monthly basis is recommended in PAH patients treated with these compounds, in order to detect an increase in the serum aminotran...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Alcohol and alcoholism

دوره 37 1  شماره 

صفحات  -

تاریخ انتشار 2002