TY - JOUR
T1 - Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids
AU - Fuentes-Broto, Lorena
AU - Martínez-Ballarín, Enrique
AU - Miana-Mena, Javier
AU - Berzosa, Cesar
AU - Piedrafita, Eduardo
AU - Cebrián, Igor
AU - Reiter, Russel J.
AU - García, Joaquín J.
N1 - Funding Information:
This work was supported by the Gobierno de Aragón (Aging and Oxidative Stress Physiology, Grant No. B40) and by F.I.S. from Instituto de Salud Carlos III (Grant No. RD06/0013/1017).
PY - 2009
Y1 - 2009
N2 - Cholestasis occurs in a variety of hepatic diseases and causes damage due to accumulation of bile acids in the liver. The aim was to investigate the effect of several bile acids, i.e. chenodeoxycholic, taurochenodeoxycholic, deoxycholic, taurodeoxycholic, ursodeoxycholic, lithocholic and taurolithocholic (TLC), in inducing oxidative damage. Hepatic tissue of male Sprague-Dawley rats was incubated with or without 1 mM of each bile acid, with or without 0.1 mM FeCl3 and 0.1 mM ascorbic acid for the purpose of generating free radicals. Several bile acids increased lipid and protein oxidation, with TLC being the most pro-oxidative (657% and 175% in homogenates and 350% and 311% in membranes, respectively). TLC also enhanced iron-induced oxidative stress to lipids (21% in homogenates and 29% in membranes) and to proteins (74% in membranes). This enhancement was dose-and time-dependent and was reduced by melatonin. These results suggest that bile acids differentially mediate hepatic oxidative stress and may be involved in the physiopathology of cholestasis.
AB - Cholestasis occurs in a variety of hepatic diseases and causes damage due to accumulation of bile acids in the liver. The aim was to investigate the effect of several bile acids, i.e. chenodeoxycholic, taurochenodeoxycholic, deoxycholic, taurodeoxycholic, ursodeoxycholic, lithocholic and taurolithocholic (TLC), in inducing oxidative damage. Hepatic tissue of male Sprague-Dawley rats was incubated with or without 1 mM of each bile acid, with or without 0.1 mM FeCl3 and 0.1 mM ascorbic acid for the purpose of generating free radicals. Several bile acids increased lipid and protein oxidation, with TLC being the most pro-oxidative (657% and 175% in homogenates and 350% and 311% in membranes, respectively). TLC also enhanced iron-induced oxidative stress to lipids (21% in homogenates and 29% in membranes) and to proteins (74% in membranes). This enhancement was dose-and time-dependent and was reduced by melatonin. These results suggest that bile acids differentially mediate hepatic oxidative stress and may be involved in the physiopathology of cholestasis.
KW - Bile acid
KW - Cholestasis
KW - Lipid peroxidation
KW - Oxidative stress
KW - Protein carbonyls
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U2 - 10.1080/10715760903176927
DO - 10.1080/10715760903176927
M3 - Article
C2 - 19669996
AN - SCOPUS:70350554282
SN - 1071-5762
VL - 43
SP - 1080
EP - 1089
JO - Free Radical Research
JF - Free Radical Research
IS - 11
ER -