Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease
Oxidative stress and hepatic mitochondria play a role in the pathogenesis of nonalcoholic fatty liver disease. The aim of the present study was to evaluate the role of hepatic mitochondrial dysfunction and oxidative stress in the pathogenesis of the disease. Fatty liver was induced in Wistar rats wi...
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2006-01-01
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doaj-054cb5a586794f50b5f637bf0f6977922020-11-24T22:46:16ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X0034-73102006-01-01392189194Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver diseaseOliveira C.P.M.S.Coelho A.M.M.Barbeiro H.V.Lima V.M.R.Soriano F.Ribeiro C.Molan N.A.T.Alves V.A.F.Souza H.P.Machado M.C.C.Carrilho F.J.Oxidative stress and hepatic mitochondria play a role in the pathogenesis of nonalcoholic fatty liver disease. The aim of the present study was to evaluate the role of hepatic mitochondrial dysfunction and oxidative stress in the pathogenesis of the disease. Fatty liver was induced in Wistar rats with a choline-deficient diet (CD; N = 7) or a high-fat diet enriched with PUFAs-omega-3 (H; N = 7) for 4 weeks. The control group (N = 7) was fed a standard diet. Liver mitochondrial oxidation and phosphorylation were measured polarographically and oxidative stress was estimated on the basis of malondialdehyde and glutathione concentrations. Moderate macrovacuolar liver steatosis was observed in the CD group and mild liver steatosis was observed in the periportal area in the H group. There was an increase in the oxygen consumption rate by liver mitochondria in respiratory state 4 (S4) and a decrease in respiratory control rate (RCR) in the CD group (S4: 32.70 ± 3.35; RCR: 2.55 ± 0.15 ng atoms of O2 min-1 mg protein-1) when compared to the H and control groups (S4: 23.09 ± 1.53, 17.04 ± 2.03, RCR: 3.15 ± 0.15, 3.68 ± 0.15 ng atoms of O2 min-1 mg protein-1, respectively), P < 0.05. Hepatic lipoperoxide concentrations were significantly increased and the concentration of reduced glutathione was significantly reduced in the CD group. A choline-deficient diet causes moderate steatosis with disruption of liver mitochondrial function and increased oxidative stress. These data suggest that lipid peroxidation products can impair the flow of electrons along the respiratory chain, causing overreduction of respiratory chain components and enhanced mitochondrial reactive oxygen species. These findings are important in the pathogenesis of nonalcoholic fatty liver disease.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2006000200004Hepatic mitochondrial dysfunctionOxidative stressNonalcoholic fatty liver diseaseCholine-deficient dietHigh-fat diet |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Oliveira C.P.M.S. Coelho A.M.M. Barbeiro H.V. Lima V.M.R. Soriano F. Ribeiro C. Molan N.A.T. Alves V.A.F. Souza H.P. Machado M.C.C. Carrilho F.J. |
spellingShingle |
Oliveira C.P.M.S. Coelho A.M.M. Barbeiro H.V. Lima V.M.R. Soriano F. Ribeiro C. Molan N.A.T. Alves V.A.F. Souza H.P. Machado M.C.C. Carrilho F.J. Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease Brazilian Journal of Medical and Biological Research Hepatic mitochondrial dysfunction Oxidative stress Nonalcoholic fatty liver disease Choline-deficient diet High-fat diet |
author_facet |
Oliveira C.P.M.S. Coelho A.M.M. Barbeiro H.V. Lima V.M.R. Soriano F. Ribeiro C. Molan N.A.T. Alves V.A.F. Souza H.P. Machado M.C.C. Carrilho F.J. |
author_sort |
Oliveira C.P.M.S. |
title |
Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
title_short |
Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
title_full |
Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
title_fullStr |
Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
title_full_unstemmed |
Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
title_sort |
liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease |
publisher |
Associação Brasileira de Divulgação Científica |
series |
Brazilian Journal of Medical and Biological Research |
issn |
0100-879X 0034-7310 |
publishDate |
2006-01-01 |
description |
Oxidative stress and hepatic mitochondria play a role in the pathogenesis of nonalcoholic fatty liver disease. The aim of the present study was to evaluate the role of hepatic mitochondrial dysfunction and oxidative stress in the pathogenesis of the disease. Fatty liver was induced in Wistar rats with a choline-deficient diet (CD; N = 7) or a high-fat diet enriched with PUFAs-omega-3 (H; N = 7) for 4 weeks. The control group (N = 7) was fed a standard diet. Liver mitochondrial oxidation and phosphorylation were measured polarographically and oxidative stress was estimated on the basis of malondialdehyde and glutathione concentrations. Moderate macrovacuolar liver steatosis was observed in the CD group and mild liver steatosis was observed in the periportal area in the H group. There was an increase in the oxygen consumption rate by liver mitochondria in respiratory state 4 (S4) and a decrease in respiratory control rate (RCR) in the CD group (S4: 32.70 ± 3.35; RCR: 2.55 ± 0.15 ng atoms of O2 min-1 mg protein-1) when compared to the H and control groups (S4: 23.09 ± 1.53, 17.04 ± 2.03, RCR: 3.15 ± 0.15, 3.68 ± 0.15 ng atoms of O2 min-1 mg protein-1, respectively), P < 0.05. Hepatic lipoperoxide concentrations were significantly increased and the concentration of reduced glutathione was significantly reduced in the CD group. A choline-deficient diet causes moderate steatosis with disruption of liver mitochondrial function and increased oxidative stress. These data suggest that lipid peroxidation products can impair the flow of electrons along the respiratory chain, causing overreduction of respiratory chain components and enhanced mitochondrial reactive oxygen species. These findings are important in the pathogenesis of nonalcoholic fatty liver disease. |
topic |
Hepatic mitochondrial dysfunction Oxidative stress Nonalcoholic fatty liver disease Choline-deficient diet High-fat diet |
url |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2006000200004 |
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