Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis

Rolo, Anabela P.; Teodoro, João S.; Palmeira, Carlos M.

doi:10.1016/j.freeradbiomed.2011.10.003

Cited by 955Liver Disease Diagnosis and TreatmentDrug-Induced Hepatotoxicity and ProtectionLiver physiology and pathology

Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis

Rolo, Anabela P., Teodoro, João S., Palmeira, Carlos M.·2012·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2011.10.003

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Abstract

The worldwide rising prevalence of obesity and insulin resistance is associated with a parallel increase in nonalcoholic fatty liver disease (NAFLD). NAFLD is characterized by excess accumulation of triglyceride in the hepatocyte due to increased inflow of free fatty acids and/or de novo lipogenesis caused by various drugs and multiple defects in energy metabolism. Accumulation of lipids in the hepatocyte impairs the oxidative capacity of the mitochondria, increasing the reduced state of the electron transport chain (ETC) complexes and stimulating peroxisomal and microsomal pathways of fat oxidation. The consequent increased generation of reactive oxygen species (ROS) and reactive aldehydic derivatives causes oxidative stress and cell death, via ATP, NAD, and glutathione depletion and DNA, lipid, and protein damage. Oxidative stress also triggers production of inflammatory cytokines, causing inflammation and a fibrogenic response. This ultimately results in the development of nonalcoholic steatohepatitis (NASH), which can result in end-stage liver disease. The current therapeutic strategies for NASH treatment are mostly directed toward correction of the risk factors. Stimulation of mitochondrial function may also prevent NASH development, protecting the cell against the increased flux of reduced substrates to the ETC and ROS generation.

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An increase in ROS generation can cause depletion of antioxidant enzymes (MnSOD, Catalase and glutathione peroxidase).
“An increase in ROS generation can cause depletion of antioxidant enzymes (MnSOD, Catalase and glutathione peroxidase).”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [9]
Depletion of antioxidant enzymes leads to formation of lipid peroxides that have detrimental effects on hepatocytes.
“This leads to formation of lipid peroxides having detrimental effects on hepatocytes [9].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [9]
Excess lipid accumulation within hepatocytes increases ROS production, as demonstrated by several in vitro and in vivo studies including the present one.
“Several in vitro and in vivo studies, including the present one, have demonstrated an increase in the ROS production as a result of excess lipid accumulation within the hepatocytes [9].”
From Intervention by picroside II on FFAs induced lipid accumulation and lipotoxicity in HepG2 cells (2021) · cites this paper as [9]
Endogenous and exogenous AGEs provoke the initiation and progression of NAFLD, and dietary AGEs from fructose- or sucrose-enriched diets and/or soft drinks can worsen liver fibrosis faster than endogenous AGEs.
“Endogenous and exogenous AGEs provoke the initiation and progression of NAFLD.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [125]
Aggregation of AGEs decreases GSH, SIRT1, and TIMP3 and increases oxidative stress and inflammation, promoting inflammatory liver injury and fibrosis in experimental animal models and NAFLD patients.
“The aggregation of AGEs decreases the levels of the most important cellular antioxidant peptides, glutathione (GSH), SIRT1, and tissue inhibitor of metalloproteinase 3 (TIMP3), accompanied by increased oxidative stress and inflammation, promoting inflammatory liver injury and fibrosis in experimental animal models and NAFLD patients55–57,124–126.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [125]

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Authors: Rolo, A. P., Teodoro, J. S., & Palmeira, C. M.
Affiliations: University of Aveiro (PT)
University of Coimbra (PT)
Corresponding author: Palmeira, Carlos M.
ORCID: Rolo, Anabela P.
Teodoro, João S.
Palmeira, Carlos M.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2012-01
Volume: 52
Issue: 1
Pages: 59-69
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2011.10.003
OpenAlex: W2061662539
Cited by: 955
References: 221
Citations by year: 2026: 39 · 2025: 51 · 2024: 56 · 2023: 73 · 2022: 58 · 2021: 74 · 2020: 68 · 2019: 75 · 2018: 73 · 2017: 66 · 2016: 67 · 2015: 70 · 2014: 78 · 2013: 76 · 2012: 27
FWCI: 6.80
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: nonalcoholic steatohepatitis, oxidative stress, non-alcoholic fatty liver disease, reactive oxygen species, mitochondrial dysfunction, electron transport chain, lipid accumulation, insulin resistance, obesity, inflammation, liver fibrosis, mitochondrial function, NAD+ depletion, glutathione depletion, end-stage liver disease
MeSH terms: Animals, DNA Damage, Fatty Acids, Nonesterified, Fatty Liver, Humans, Inflammation, Insulin Resistance, Mitochondria, Oxidation-Reduction, Triglycerides, Lipid Peroxidation, Cytokines, Reactive Oxygen Species, Oxidative Stress, Hepatocytes, Mice, Rats, Proteolysis, Non-alcoholic Fatty Liver Disease

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Role of oxidative stress in the pathogenesis of nonalcoholic steatohepatitis

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