ArticleToxics2023
Lipidomics Analysis Explores the Mechanism of Renal Injury in Rat Induced by 3-MCPD.
Article in Toxics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 7 citations in OpenAlex.
- Decoding the Sphingolipid Landscape of Clear Cell Renal Cell Carcinoma: A Single-Cell-Guided Prognostic Model Built With 101 Machine Learning.Human mutation · 2026Article
- Boric Acid and Borax Protect Human Lymphocytes from Oxidative Stress and Genotoxicity Induced by 3-Monochloropropane-1,2-diol.Biological trace element research · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
3-monochloropropane-1,2-diol (3-MCPD) is a food-process toxic substance, and its main target organ is the kidney. The present study examined and characterized the nephrotoxicity and the lipidomic mechanisms in a model of kidney injury in Sprague Dawley (SD) rats treated with high (45 mg/kg) and low (30 mg/kg) doses of 3-MCPD. The results showed that the ingestion of 3-MCPD led to a dose-dependent increase in serum creatinine and urea nitrogen levels and histological renal impairment. The oxidative stress indicators (MDA, GSH, T-AOC) in the rat kidney altered in a dose-dependent manner in 3-MCPD groups. The lipidomics analysis revealed that 3-MCPD caused kidney injury by interfering with glycerophospholipid metabolism and sphingolipid metabolism. In addition, 38 lipids were screened as potential biomarkers. This study not only revealed the mechanism of 3-MCPD renal toxicity from the perspective of lipidomics but also provided a new approach to the study of 3-MCPD nephrotoxicity.
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Registered trials
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