ArticleToxicology and applied pharmacology2014
Differential metabolism of 4-hydroxynonenal in liver, lung and brain of mice and rats.
Article in Toxicology and applied pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Toxic aldehydes in cooking vegetable oils: Generation, toxicity and disposal methods.Food chemistry: X · 2025Review
- Cleavage of Hsp70.1 causes lysosomal cell death under stress conditions.Frontiers in molecular biosciences · 2024Review
- Response of a Human Lens Epithelial Cell Line to Hyperglycemic and Oxidative Stress: The Role of Aldose Reductase.Antioxidants (Basel, Switzerland) · 2023Article
- A time differentiated dietary intervention effect on the biomarkers of exposure to pyrethroids and neonicotinoids pesticides.iScience · 2023Article
- Electrophilic Aldehyde 4-Hydroxy-2-Nonenal Mediated Signaling and Mitochondrial Dysfunction.Biomolecules · 2022Review
- Article
- Involvement of 4-hydroxy-2-nonenal in the pathogenesis of pulmonary fibrosis.Molecular and cellular biochemistry · 2021Review
- Article
- Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression.PloS one · 2021Article
- ORY supplementation mitigates acetaminophen-induced acute liver failure in male mice: role of oxidative stress and apoptotic markers.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Can Medicinal Plants and Bioactive Compounds Combat Lipid Peroxidation Product 4-HNE-Induced Deleterious Effects?Biomolecules · 2020Review
- Dual Substance Use of Electronic Cigarettes and Alcohol.Frontiers in physiology · 2020Review
- Electrophile Signaling and Emerging Immuno- and Neuro-modulatory Electrophilic Pharmaceuticals.Frontiers in aging neuroscience · 2020Article
- Silibinin ameliorates hepatic lipid accumulation and oxidative stress in mice with non-alcoholic steatohepatitis by regulating CFLAR-JNK pathway.Acta pharmaceutica Sinica. B · 2019Article
- 4-Hydroxy-Trans-2-Nonenal in the Regulation of Anti-Oxidative and Pro-Inflammatory Signaling Pathways.Oxidative medicine and cellular longevity · 2019Review
- Growth of Triple Negative and Progesterone Positive Breast Cancer Causes Oxidative Stress and Down-Regulates Neuroprotective Transcription Factor NPAS4 and NPAS4-Regulated Genes in Hippocampal Tissues of TumorGraft Mice-an Aging Connection.Frontiers in genetics · 2018Article
- Signaling by 4-hydroxy-2-nonenal: Exposure protocols, target selectivity and degradation.Archives of biochemistry and biophysics · 2017Review
- Alcohol, Aldehydes, Adducts and Airways.Biomolecules · 2015Review
- Oxidative stress in severe acute illness.Redox biology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The lipid peroxidation end-product 4-hydroxynonenal (4-HNE) is generated in tissues during oxidative stress. As a reactive aldehyde, it forms Michael adducts with nucleophiles, a process that disrupts cellular functioning. Liver, lung and brain are highly sensitive to xenobiotic-induced oxidative stress and readily generate 4-HNE. In the present studies, we compared 4-HNE metabolism in these tissues, a process that protects against tissue injury. 4-HNE was degraded slowly in total homogenates and S9 fractions of mouse liver, lung and brain. In liver, but not lung or brain, NAD(P)+ and NAD(P)H markedly stimulated 4-HNE metabolism. Similar results were observed in rat S9 fractions from these tissues. In liver, lung and brain S9 fractions, 4-HNE formed protein adducts. When NADH was used to stimulate 4-HNE metabolism, the formation of protein adducts was suppressed in liver, but not lung or brain. In both mouse and rat tissues, 4-HNE was also metabolized by glutathione S-transferases. The greatest activity was noted in livers of mice and in lungs of rats; relatively low glutathione S-transferase activity was detected in brain. In mouse hepatocytes, 4-HNE was rapidly taken up and metabolized. Simultaneously, 4-HNE-protein adducts were formed, suggesting that 4-HNE metabolism in intact cells does not prevent protein modifications. These data demonstrate that, in contrast to liver, lung and brain have a limited capacity to metabolize 4-HNE. The persistence of 4-HNE in these tissues may increase the likelihood of tissue injury during oxidative stress.
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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.