Coenzyme Q in pregnant women and rats with intrahepatic cholestasis

MARTINEFSKI M; CONTIN M; RODRIGUEZ MR; GERÉZ E; GALLEANO M; LUCANGIOLI S; BIANCIOTTI LG; TRIPODI V

LIVER INTERNATIONAL

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2014 p. 1040 - 1048

1478-3223

Background and aims: Intrahepatic cholestasis of pregnancy is a high risk liver diseasegiven the eventual deleterious consequences that may occur in the fetus. It is accepted thatthe abnormal accumulation of hydrophobic bile acids in maternal serum are responsible forthe disease development. Hydrophobic bile acids induce oxidative stress and apoptosisleading to the damage of the hepatic parenchyma and eventually extrahepatic tissues. Ascoenzyme Q (CoQ) is considered an early marker of oxidative stress in the present studywe sought to assess CoQ levels, bile acid profile, and oxidative stress status in intrahepaticcholestasis. Methods: CoQ, vitamin E and malondialdehyde were measured in plasmaand/or tissues by HPLC-UV method whereas serum bile acids by capillary electrophoresisin rats with ethinyl estradiol-induced cholestasis and women with pregnancy cholestasis.Results: CoQ and vitamin E plasma levels were diminished in both rats and women withintrahepatic cholestasis. Furthermore reduced CoQ was also found in muscle and brain ofcholestatic rats but no changes were observed in heart or liver. In addition, a positivecorrelation between CoQ and ursodeoxycholic/lithocholic acid ratio was found inintrahepatic cholestasis suggesting that increased plasma lithocholic acid may be intimatelyrelated to CoQ depletion in blood and tissues.Conclusion: Significant CoQ and vitamin E depletion occur in both animals and humanswith intrahepatic cholestasis likely as the result of increased hydrophobic bile acids knownto produce significant oxidative stress. Present findings further suggest that antioxidantsupplementation complementary to traditional treatment may improve cholestasis outcome.