ArticleHepatology international2008
Effects of S-adenosylmethionine on liver methionine metabolism and steatosis with ethanol-induced liver injury in rats.
Article in Hepatology international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 94 citations in OpenAlex.
- Alcoholic liver disease patients treated with S-adenosyl-L-methionine: an in-depth look at liver morphologic data comparing pre and post treatment liver biopsies.Experimental and molecular pathology · 2013Trial
- l-Cysteine-Glutathione Mixed Disulfide, a Novel Bioavailable Sulfhydryl-Modified Glutathione Precursor, Protects against Early Liver Injury Induced by Short-Term Hypercholesterolemia.Chemical research in toxicology · 2025Article
- Amelioration effects of the soybean lecithin-gallic acid complex on iron-overload-induced oxidative stress and liver damage in C57BL/6J mice.Pharmaceutical biology · 2023Article
- A decrease in NR2B expression mediated by DNA hypermethylation induces perioperative neurocognitive disorder in aged mice.CNS neuroscience & therapeutics · 2023Article
- Review
- Nrf2 mediates the protective effects of homocysteine by increasing the levels of GSH content in HepG2 cells.Molecular medicine reports · 2017Article
- Laboratory models available to study alcohol-induced organ damage and immune variations: choosing the appropriate model.Alcoholism, clinical and experimental research · 2010Review
- The cyclic pattern of blood alcohol levels during continuous ethanol feeding in rats: the effect of feeding S-adenosylmethionine.Experimental and molecular pathology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperhomocysteinemia is implicated in the pathogenesis of various liver diseases. In this study, the effects of S-adenosylmethionine (SAM) on hyperhomocysteinemia and steatosis with ethanol-induced liver injury in rats were examined and their mechanisms were explored.
methodsForty-eight female Sprague-Dawley rats were randomly divided into four groups as control, model, low-dose, and high-dose SAM groups. Except the control group, all rats were fed high-fat-containing diet plus ethanol and fish oil gavaged for 8 weeks. SAM was administered by intraperitoneal injection after the 4 weeks' exposure of ethanol. Serum homocysteine (Hcy), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta1 (TGF-beta1) levels were determined. The contents of liver malondialdehyde (MDA) and glutathione (GSH) were assayed. Liver histology was also examined. The expressions of TNF-alpha and TGF-beta1 mRNAs in the liver were detected by the reverse transcriptase-polymerase chain reaction assay.
resultsCompared with the control group, the model group rats developed marked liver damage, accompanied by an increase in Hcy, ALT, AST, TC, TG, TNF-alpha, TGF-beta1, and MDA levels. However, the levels of GSH were decreased. These responses were associated with the increased expression of TNF-alpha and TGF-beta1 mRNAs in the livers, as well as the existence of hepatocellular necrosis and neutrophil infiltration in the livers. In treatment groups, SAM provided significant protection from the liver injury induced by alcohol, resulting in a decrease in serum TNF-alpha, TGF-beta1 levels, lipid peroxidation, and the expressions of TNF-alpha and TGF-beta1 mRNAs in the livers, as well as an increase in GSH levels. However, no statistical difference was observed in these parameters between the two different dose treatment groups. In the study, SAM did not affect plasma total homocysteine (tHcy) levels significantly.
conclusionSAM prevents alcohol-induced liver injury in rats by reducing liver lipid peroxidation, anti-inflammation, and antihyperplasia. In addition, it does not affect the plasma tHcy levels.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.