ArticleToxicology and applied pharmacology2011
Oxidative stress and hepatic stellate cell activation are key events in arsenic induced liver fibrosis in mice.
Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 148 citations in OpenAlex.
- PLGA-loaded puerarin attenuates arsenic-induced liver injury through modulation of ferroptosis, oxidative stress, inflammation, and apoptotic signaling.BMC pharmacology & toxicology · 2026Article
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- Toxicology of Airborne Inorganic Arsenic: Oxidative Stress, Molecular Mechanisms, and Organ-Specific Pathologies.Toxics · 2025Review
- Targeting Lipophagy in Liver Diseases: Impact on Oxidative Stress and Steatohepatitis.Antioxidants (Basel, Switzerland) · 2025Review
- Chronic Exposure to Arsenic and Fluoride Starting at Gestation Alters Liver Mitochondrial Protein Expression and Induces Early Onset of Liver Fibrosis in Male Mouse Offspring.Biological trace element research · 2025Article
- Sotagliflozin Modulation of SIRT1/Nrf2 and PI3K/AKT Signaling Pathway Ameliorates Experimental Liver Fibrosis in Rats.Oxidative medicine and cellular longevity · 2025Article
- Hepatoprotective Potential ofCurrent drug discovery technologies · 2025Review
- The role of Juniperus Macrocarpa extract as anti-inflammatory and antioxidant on methotrexate-induced acute liver injury in rat model.F1000Research · 2025Article
- Hepatotoxicity induced by arsenic trioxide: clinical features, mechanisms, preventive and potential therapeutic strategies.Frontiers in pharmacology · 2025Review
- Leveraging the One Health concept for arsenic sustainability.Eco-Environment & Health · 2024Review
- Arsenic toxicity: sources, pathophysiology and mechanism.Toxicology research · 2024Review
- PTEN Overexpression Alters Autophagy Levels and Slows Sodium Arsenite-Induced Hepatic Stellate Cell Fibrosis.Toxics · 2023Article
- Human umbilical cord blood mesenchymal stem cells as a potential therapy for schistosomal hepatic fibrosis: an experimental study.Pathogens and global health · 2023Article
- Nanodrug rescues liver fibrosis via synergistic therapy with HCommunications biology · 2023Article
- Pathophysiological mechanisms of hepatic stellate cells activation in liver fibrosis.World journal of clinical cases · 2022Review
- In vitro toxic interaction of arsenic and hyperglycemia in mitochondria: an important implication of increased vulnerability in pre-diabetics.Environmental science and pollution research international · 2022Article
- Traditional Chinese medicine: An important source for discovering candidate agents against hepatic fibrosis.Frontiers in pharmacology · 2022Review
- Exploration of the Components and Pharmacological Mechanisms of Keyin Pill-Induced Liver Injury Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Arsenic-Induced Injury of Mouse Hepatocytes through Lysosome and Mitochondria: An In Vitro Study.International journal of hepatology · 2022Article
- Molecular Mechanisms and Potential New Therapeutic Drugs for Liver Fibrosis.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Arsenic is an environmental toxicant and carcinogen. Exposure to arsenic is associated with development of liver fibrosis and portal hypertension through ill defined mechanisms. We evaluated hepatic fibrogenesis after long term arsenic exposure in a murine model. BALB/c mice were exposed to arsenic by daily gavages of 6 μg/gm body weight for 1 year and were evaluated for markers of hepatic oxidative stress and fibrosis, as well as pro-inflammatory, pro-apoptotic and pro-fibrogenic factors at 9 and 12 months. Hepatic NADPH oxidase activity progressively increased in arsenic exposure with concomitant development of hepatic oxidative stress. Hepatic steatosis with occasional collection of mononuclear inflammatory cells and mild portal fibrosis were the predominant liver lesion observed after 9 months of arsenic exposure, while at 12 months, the changes included mild hepatic steatosis, inflammation, necrosis and significant fibrosis in periportal areas. The pathologic changes in the liver were associated with markers of hepatic stellate cells (HSCs) activation, matrix reorganization and fibrosis including α-smooth muscle actin, transforming growth factor-β1, PDGF-Rβ, pro-inflammatory cytokines and enhanced expression of tissue inhibitor of metalloproteinase-1 and pro(α) collagen type I. Moreover, pro-apoptotic protein Bax was dominantly expressed and Bcl-2 was down-regulated along with increased number of TUNEL positive hepatocytes in liver of arsenic exposed mice. Furthermore, HSCs activation due to increased hepatic oxidative stress observed after in vivo arsenic exposure was recapitulated in co-culture model of isolated HSCs and hepatocytes exposed to arsenic. These findings have implications not only for the understanding of the pathology of arsenic related liver fibrosis but also for the design of preventive strategies in chronic arsenicosis.
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Registered trials
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