ArticleJournal of applied toxicology : JAT2022
Phosphatidylcholine (18:0/20:4), a potential biomarker to predict ethionamide-induced hepatic steatosis in rats.
Article in Journal of applied toxicology : JAT, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Maximizing Lipidome Coverage of Mouse Liver Following the IV Administration of Gefitinib by Combining Both UHPLC-MS-Based Untargeted and Targeted Lipidomics.Journal of proteome research · 2026Article
- The study of immunological markers in tuberculosis across animal models and its translation to human research.Lab animal · 2026Review
- Lecithin exerts direct lipid-lowering and antioxidant cytoprotective effectsFrontiers in physiology · 2026Article
- Plasma metabolites as potential markers and targets to prevent and treat urolithiasis: a Mendelian randomization study.Frontiers in molecular biosciences · 2024Article
- Phosphatidylcholine (18:0/20:4), a potential biomarker to predict ethionamide-induced hepatic steatosis in rats.Journal of applied toxicology : JAT · 2022Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
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Abstract
Ethionamide (ETH), a second-line drug for multidrug-resistant tuberculosis, is known to cause hepatic steatosis in rats and humans. To investigate predictive biomarkers for ETH-induced steatosis, we performed lipidomics analysis using plasma and liver samples collected from rats treated orally with ETH at 30 and 100 mg/kg for 14 days. The ETH-treated rats developed hepatic steatosis with Oil Red O staining-positive vacuolation in the centrilobular hepatocytes accompanied by increased hepatic contents of triglycerides (TG) and decreased plasma TG and total cholesterol levels. A multivariate analysis for lipid profiles revealed differences in each of the 35 lipid species in the plasma and liver between the control and the ETH-treated rats. Of those lipids, phosphatidylcholine (PC) (18:0/20:4) decreased dose-dependently in both the plasma and liver. Moreover, serum TG-rich very low-density lipoprotein (VLDL) levels, especially the large particle fraction of VLDL composed of PC containing arachidonic acid (20:4) involved in hepatic secretion of TG, were decreased dose-dependently. In conclusion, the decreased PC (18:0/20:4) in the liver, possibly leading to suppression of hepatic TG secretion, was considered to be involved in the pathogenesis of the ETH-induced hepatic steatosis. Therefore, plasma PC (18:0/20:4) levels are proposed as mechanism-related biomarkers for ETH-induced hepatic steatosis.
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