Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids

Lorena Fuentes-Broto, Enrique Martínez-Ballarín, Javier Miana-Mena, Cesar Berzosa, Eduardo Piedrafita, Igor Cebrián, Russel J Reiter, Joaquín J. García

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1080-1089
Number of pages10
JournalFree Radical Research
Volume43
Issue number11
DOIs
StatePublished - 2009

Fingerprint

Cell membranes
Bile Acids and Salts
Hepatocytes
Cell Membrane
Lipids
Oxidation
Oxidative stress
Liver
Cholestasis
Proteins
Membranes
Oxidative Stress
Melatonin
Ascorbic Acid
Free Radicals
Sprague Dawley Rats
Rats
Membrane Proteins
Iron
Tissue

Keywords

  • Bile acid
  • Cholestasis
  • Lipid peroxidation
  • Oxidative stress
  • Protein carbonyls

ASJC Scopus subject areas

  • Biochemistry
  • Medicine(all)

Cite this

Fuentes-Broto, L., Martínez-Ballarín, E., Miana-Mena, J., Berzosa, C., Piedrafita, E., Cebrián, I., ... García, J. J. (2009). Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids. Free Radical Research, 43(11), 1080-1089. https://doi.org/10.1080/10715760903176927

Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids. / Fuentes-Broto, Lorena; Martínez-Ballarín, Enrique; Miana-Mena, Javier; Berzosa, Cesar; Piedrafita, Eduardo; Cebrián, Igor; Reiter, Russel J; García, Joaquín J.

In: Free Radical Research, Vol. 43, No. 11, 2009, p. 1080-1089.

Research output: Contribution to journalArticle

Fuentes-Broto, L, Martínez-Ballarín, E, Miana-Mena, J, Berzosa, C, Piedrafita, E, Cebrián, I, Reiter, RJ & García, JJ 2009, 'Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids', Free Radical Research, vol. 43, no. 11, pp. 1080-1089. https://doi.org/10.1080/10715760903176927
Fuentes-Broto L, Martínez-Ballarín E, Miana-Mena J, Berzosa C, Piedrafita E, Cebrián I et al. Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids. Free Radical Research. 2009;43(11):1080-1089. https://doi.org/10.1080/10715760903176927
Fuentes-Broto, Lorena ; Martínez-Ballarín, Enrique ; Miana-Mena, Javier ; Berzosa, Cesar ; Piedrafita, Eduardo ; Cebrián, Igor ; Reiter, Russel J ; García, Joaquín J. / Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids. In: Free Radical Research. 2009 ; Vol. 43, No. 11. pp. 1080-1089.
@article{884dfc4dbfcf4f36bb1e1fe7e1eaca3c,
title = "Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids",
abstract = "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.",
keywords = "Bile acid, Cholestasis, Lipid peroxidation, Oxidative stress, Protein carbonyls",
author = "Lorena Fuentes-Broto and Enrique Mart{\'i}nez-Ballar{\'i}n and Javier Miana-Mena and Cesar Berzosa and Eduardo Piedrafita and Igor Cebri{\'a}n and Reiter, {Russel J} and Garc{\'i}a, {Joaqu{\'i}n J.}",
year = "2009",
doi = "10.1080/10715760903176927",
language = "English (US)",
volume = "43",
pages = "1080--1089",
journal = "Free Radical Research",
issn = "1071-5762",
publisher = "Informa Healthcare",
number = "11",

}

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.

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

UR - http://www.scopus.com/inward/record.url?scp=70350554282&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70350554282&partnerID=8YFLogxK

U2 - 10.1080/10715760903176927

DO - 10.1080/10715760903176927

M3 - Article

VL - 43

SP - 1080

EP - 1089

JO - Free Radical Research

JF - Free Radical Research

SN - 1071-5762

IS - 11

ER -