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Updated: Jun 23, 2026

Methods for Analyzing the Impacts of Natural Uranium on In Vitro Osteoclastogenesis
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In Vitro hRPTEC TERT1 Model for Uranium-Induced Nephrotoxicity Pathway Study.

Marie Frerejacques1, Victoria Powell1, Sebastien Giraud2

  • 1LRSI, SESANE, PSE-SANTE, Nuclear Safety and Radiation Protection Authority (ASNR), Fontenay-aux-Roses, 92262, France.

Journal of Toxicology
|June 22, 2026
PubMed
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This summary is machine-generated.

Uranium (U(VI)) causes kidney toxicity through oxidative stress and inflammation. This study details the adverse outcome pathway (AOP) for uranium-induced renal failure using human kidney cells, identifying key molecular events.

Area of Science:

  • Toxicology and Pharmacology
  • Renal Cell Biology
  • Environmental Health

Background:

  • Uranium (U(VI)), a heavy metal and alpha emitter, poses significant chemical and radiological toxicity risks, primarily targeting the kidneys.
  • The precise mechanisms of uranium-induced renal failure remain incompletely understood, particularly through the lens of the Adverse Outcome Pathway (AOP) approach.
  • Understanding these mechanisms is crucial for developing effective strategies to mitigate uranium's nephrotoxic effects.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying uranium (U(VI))-induced kidney toxicity using an in vitro model of human renal proximal tubule epithelial cells (hRPTEC TERT1).
  • To contribute to the development of the Adverse Outcome Pathway (AOP) for kidney toxicity.
  • To identify key events at the gene and protein levels associated with uranium exposure, including oxidative stress, apoptosis, inflammation, and cell survival.
Keywords:
adverse outcome pathwayhRPTEC TERT1 cellsnephrotoxicityuranium

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Main Methods:

  • Utilized a specialized in vitro model of human renal proximal tubule epithelial cells (hRPTEC TERT1).
  • Determined U(VI) concentrations inducing apoptosis (Caspase 3/7 activity) and necrosis (LDH assay).
  • Analyzed gene and protein expression levels related to oxidative stress (ROS), apoptosis, cell survival, inflammation (TNFα, IL-6, IL-18), and kidney injury biomarkers (KIM-1).

Main Results:

  • Apoptosis was induced from 300 μM U(VI), and necrosis from 500 μM, with an IC50 of 420 μM after 48h exposure.
  • Uranium exposure led to early oxidative stress (ROS production) and subsequent antioxidant responses.
  • Higher U(VI) concentrations (> 300 μM) triggered significant inflammatory responses and increased caspase 3/7 and LDH activities, with a slight increase in KIM-1 protein.

Conclusions:

  • This study successfully generated a multiplex panel detailing key events in the AOP of uranium-induced renal failure using a relevant human kidney cell model.
  • The findings elucidate the dose-dependent effects of U(VI) on renal cells, highlighting oxidative stress and inflammation as critical contributors to nephrotoxicity.
  • This research provides a foundation for further investigation into uranium's renal toxicity and the development of targeted interventions.