Paper
Effects of the lipidperoxidation product 4-hydroxynonenal and related aldehydes on proliferation and viability of cultured Ehrlich ascites tumor cells.
Published Nov 1, 1985 · S. Hauptlorenz, H. Esterbauer, W. Moll
Biochemical pharmacology
Q1 SJR score
109
Citations
0
Influential Citations
Abstract
Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.
In Vitro Study
Highly CitedStudy Snapshot
4-hydroxynonenal and related aldehydes inhibit the growth of cultured Ehrlich ascites tumor cells by blocking DNA synthesis, but do not cause cell death.
PopulationOlder adults (50-71 years)
Sample size24
MethodsObservational
OutcomesBody Mass Index projections
ResultsSocial networks mitigate obesity in older groups.
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References
Metabolism of the lipid peroxidation product 4-hydroxynonenal by isolated hepatocytes and by liver cytosolic fractions.
Hepatocytes and rat liver cytosol rapidly convert 4-hydroxynonenal into the less toxic alcohol non-2-ene-1,4-diol, potentially playing a role in general defense against oxidative stress.
1985·217citations·H. Esterbauer et al.·The Biochemical journal
The Biochemical journal
Separation and characterization of the aldehydic products of lipid peroxidation stimulated by carbon tetrachloride or ADP-iron in isolated rat hepatocytes and rat liver microsomal suspensions.
Lipid peroxidation pathways in rat livers are different, with ADP-iron being more effective in producing malonaldehyde and other carbonyl products, but both CCl4 and ADP-iron stimulate malonaldehyde production.
1985·346citations·G. Poli et al.·The Biochemical journal
The Biochemical journal
4‐Hydroxyalk‐2‐enals are substrates for glutathione transferase
Glutathione transferases play a major role in protecting cells from oxidative damage caused by products of lipid peroxidation, such as 4-hydroxyalk-2-enals.
1985·396citations·P. Ålin et al.·FEBS Letters
FEBS Letters
Inhibition of protein synthesis by carbonyl compounds (4-hydroxyalkenals) originating from the peroxidation of liver microsomal lipids.
Carbonyl compounds released during liver microsomal lipid peroxidation inhibit protein synthesis, likely due to interactions with essential SH groups in the cellular protein synthesizing machinery.
1981·65citations·A. Benedetti et al.·Chemico-biological interactions
Chemico-biological interactions
Identification of 4-hydroxynonenal as a cytotoxic product originating from the peroxidation of liver microsomal lipids.
4-hydroxynonenal, a cytotoxic substance, is formed during NADPH-Fe stimulated peroxidation of liver microsomal lipids, potentially explaining lipid peroxidation's deleterious effects on cells.
1980·703citations·A. Benedetti et al.·Biochimica et biophysica acta
Biochimica et biophysica acta
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n‐6 and n‐3 Fatty acids and their metabolites augment inhibitory action of doxorubicin on the proliferation of human neuroblastoma (IMR‐32) cells by enhancing lipid peroxidation and suppressing Ras, Myc, and Fos
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BioFactors
Genotoxicity of lipid oxidation compounds
Lipid peroxidation compounds, particularly 4-hydroxynonenal, can cause DNA damage and cell death, with their genotoxic properties affecting pathophysiological development.
2017·62citations·P. Eckl et al.·Free Radical Biology and Medicine
Free Radical Biology and Medicine
Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated Colorectal Cancer
Oxidative stress and secondary carbonyl lesions play a crucial role in the development and progression of ulcerative colitis and colitis-associated colorectal cancer.
2015·170citations·Zhiqi Wang et al.·Oxidative Medicine and Cellular Longevity
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