ArticleWorld journal of gastroenterology2017
Reabsorption of iron into acutely damaged rat liver: A role for ferritins.
Article in World journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Adipose-Derived Mesenchymal Stem Cells Improve Acute Liver Injury: A Mechanistic Study Based on the TLR4/MyD88/NF-κB Pathway.International journal of molecular sciences · 2025Article
- Study on ferritin and liver injury in pediatric hemophagocytic lymphohistiocytosis associated with infection.Scientific reports · 2025Article
- Identification of iron metabolism-related key genes and exploration of their potential mechanisms in hemophagocytic lymphohistiocytosis based on transcriptome sequencing.Frontiers in medicine · 2025Article
- Sex-dependent effects of long-term clozapine or haloperidol medication on red blood cells and liver iron metabolism in Sprague Dawley rats as a model of metabolic syndrome.BMC pharmacology & toxicology · 2022Article
- Resveratrol ameliorates iron overload induced liver fibrosis in mice by regulating iron homeostasis.PeerJ · 2022Article
- Differential response to a 6-month energy-restricted treatment depending on SH2B1 rs7359397 variant in NAFLD subjects: Fatty Liver in Obesity (FLiO) Study.European journal of nutrition · 2021Article
- Adverse effects of iron deficiency anemia on pregnancy outcome and offspring development and intervention of three iron supplements.Scientific reports · 2021Article
- PECAM-1 modulates liver damage induced by synergistic effects of TNF-α and irradiation.Journal of cellular and molecular medicine · 2019Article
- Iron-Induced Liver Injury: A Critical Reappraisal.International journal of molecular sciences · 2019Review
- Protective Role of Histidine Supplementation Against Oxidative Stress Damage in the Management of Anemia of Chronic Kidney Disease.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Mediators of hypoxia in a rat model of sterile-induced acute liver injury.International journal of clinical and experimental pathology · 2017Article
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Authors and funding
4 authors at 4 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo studied iron metabolism in liver, spleen, and serum after acute liver-damage, in relation to surrogate markers for liver-damage and repair.
methodsRats received intraperitoneal injection of the hepatotoxin thioacetamide (TAA), and were sacrificed regularly between 1 and 96 h thereafter. Serum levels of transaminases and iron were measured using conventional laboratory assays. Liver tissue was used for conventional histology, immunohistology, and iron staining. The expression of acute-phase cytokines, ferritin light chain (FTL), and ferritin heavy chain (FTH) was investigated in the liver by qRT-PCR. Western blotting was used to investigate FTL and FTH in liver tissue and serum. Liver and spleen tissue was also used to determine iron concentrations.
resultsAfter a short initial decrease, iron serum concentrations increased in parallel with serum transaminase (aspartate aminotransferase and alanine aminotransferase) levels, which reached a maximum at 48 h, and decreased thereafter. Similarly, after 48 h a significant increase in FTL, and after 72h in FTH was detected in serum. While earliest morphological signs of inflammation in liver were visible after 6 h, increased expression of the two acute-phase cytokines IFN-γ (1h) and IL-1β (3h) was detectable earlier, with maximum values after 12-24 h. Iron concentrations in liver tissue increased steadily between 1 h and 48 h, and remained high at 96 h. In contrast, spleen iron concentrations remained unchanged until 48 h, and increased mildly thereafter (96 h). Although tissue iron staining was negative, hepatic FTL and FTH protein levels were strongly elevated. Our results reveal effects on hepatic iron concentrations after direct liver injury by TAA. The increase of liver iron concentrations may be due to the uptake of a significant proportion of the metal by healthy hepatocytes, and only to a minor extent by macrophages, as spleen iron concentrations do not increase in parallel. The temporary increase of iron, FTH and transaminases in serum is obviously due to their release by damaged hepatocytes.
conclusionIncreased liver iron levels may be the consequence of hepatocyte damage. Iron released into serum by damaged hepatocytes is obviously transported back and stored via ferritins.
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