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Updated: Aug 23, 2026

An In Ovo Model for Testing Insulin-mimetic Compounds
Published on: April 23, 2018
The permeability and cytotoxicity of insulin-mimetic vanadium compounds
Xiao-Gai Yang1, Xiao-Da Yang, Lan Yuan
1Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University, Beijing 100083, China. xyang@bjmu.edu.cn
Purpose:
The aim of this study was to investigate the mechanism of permeation and cytotoxicity of vanadium compounds, [VO(acac)2], [VO(ma)2], and vanadate.
Methods:
Absorptive transport were carried out in Caco-2 monolayers grown on transwell inserts. Vanadium was quantified using inductively coupled plasma atomic emission spectrometry (ICP-AES). The change of Caco-2 cells in the microvilli morphology and F-actin structure was visualized by transmission electron microscopy and confocal laser scanning microscopy.
Results:
The three vanadium compounds were taken up by Caco-2 cells via simple passive diffusion. [VO(acac)2] were mainly transcellularly transported and exhibited the highest apparent permeabilty coefficients (8.2 x 10(-6) cm(-1)). The cell accumulation of [VO(acac)2] was found to be greater than that of [VO(ma)2], and vanadate caused much less accumulation than the other two compounds. Vanadium compounds induced intracellular reactive oxygen species, reduced the transepithelial electric resistance, caused morphological change in microvilli, and led to different perturbation of F-actin structure.
Conclusions:
The three compounds exhibited different permeability due to different diffusion process and cellular uptake. The toxicity of vanadium complexes on Caco-2 monolayer involved F-actin-related change of tight junction and impairment of microvilli. The toxicity was also related to elevated intracellular reactive oxygen species (ROS) and their cellular accumulation.
Insights
Vanadium compounds permeate Caco-2 cells via passive diffusion, with varying cell accumulation and toxicity. Their effects involve reactive oxygen species, tight junction changes, and microvilli impairment.
Area of Science:
- Biochemistry
- Cell Biology
- Toxicology
Background:
- Vanadium compounds are increasingly studied for their biological effects.
- Understanding their transport and toxicity is crucial for risk assessment.
Purpose of the Study:
- To investigate the permeation mechanisms of vanadium compounds ([VO(acac)2], [VO(ma)2], vanadate) in Caco-2 cells.
- To evaluate the cytotoxicity of these vanadium compounds.
Main Methods:
- Caco-2 cell monolayers were used to study absorptive transport.
- Vanadium levels were quantified using inductively coupled plasma atomic emission spectrometry (ICP-AES).
- Cellular morphology and F-actin structure were examined using electron and confocal microscopy.
Main Results:
- Vanadium compounds were absorbed via passive diffusion.
- [VO(acac)2] showed the highest permeability and cell accumulation.
- Vanadium exposure induced reactive oxygen species, reduced electrical resistance, and altered cell structure.
Conclusions:
- Permeability and uptake varied among vanadium compounds due to diffusion and cellular processes.
- Vanadium toxicity involved F-actin disruption, tight junction changes, microvilli impairment, and elevated ROS.
- Cellular accumulation of vanadium correlated with observed toxicity.
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