Tartrazine and blood vessel formation in zebrafish and human cells
What it found
In zebrafish embryos and human cells grown in the lab, tartrazine disrupted the formation of blood vessels.
The dye caused bleeding in zebrafish and stopped human endothelial cells from multiplying, moving and forming tubes.
What they found
Animal and lab studies
Bleeding in zebrafish
Tartrazine caused bleeding in zebrafish embryos in a dose-dependent way, starting at 2 days after fertilisation. At lower doses the bleeding appeared around the duct of Cuvier, and at higher doses it spread to other parts of the body including the brain.
Blood vessel defects in fish
In transgenic zebrafish, tartrazine disrupted the organisation of endothelial cells into vessels, especially in the sub-intestinal vein and brain area. The dorsal lateral anastomosis vessels and intersegmental vessels were only marginally affected.
Human cell growth
Tartrazine stopped human umbilical vein endothelial cells from multiplying, with an IC50 of 30 mg/L. The effect was dose-dependent and significant even at the lowest dose tested, 10.7 mg/L.
Human cell tube formation
Tartrazine stopped human endothelial cells from forming tubes and branches in the lab. Tubes and branches stopped forming completely at 267 mg/L.
Human cell movement
Tartrazine substantially stopped human endothelial cells from moving in a wound healing test. This effect was also dose-dependent.
Other findings
Possible mechanism
The authors suggest tartrazine may work by interfering with Rho family GTPase pathways, which control the cell skeleton. A computer prediction found that human RAC1 protein could interact with tartrazine.
What the authors conclude
“Taken together, our results indicate for the first time that TTZ can affect endothelial cell properties, possibly by disrupting Rho family GTPase pathways which control the cytoskeleton.”
Also in their conclusions
- They say this is the first study to report that tartrazine has vascular disrupting properties.
- They suggest the dye may affect blood vessel formation by interacting with the BMP pathway rather than the VEGF-A pathway.
- They say the newly found anti-angiogenic feature may explain the purpura experienced by some individuals, which has long been attributed to an immune response.
How it was done
Tartrazine is a widely used food colouring whose effects on human health are still debated. The authors wanted to see whether it could affect the blood vessel system, which had not been reported before.
They exposed zebrafish embryos to tartrazine from 3 to 4 hours after fertilisation until 4 days, and looked at blood vessel development using fluorescent fish. They also treated human umbilical vein endothelial cells with tartrazine and measured their growth, tube formation and movement.
What it can’t tell you
- These are zebrafish embryos and human cells grown in the lab. They cannot show what happens in a person who eats tartrazine.
- The study does not show whether tartrazine reaches the blood vessels at levels that would cause these effects in people.
- The exact mechanism by which tartrazine disrupts blood vessels is not yet known.
Who paid
- Funding
- Funded by Wallonie-Bruxelles International; Fonds De La Recherche Scientifique - FNRS (from the PubMed record).
- Conflicts
- Declarations. Competing interests: The authors declare no competing interests.
- Authors work at
- Université de Liège, Belgium; VNU University of Science, Vietnam; Vietnam National University, Vietnam
The paper
- Title
- The food dye Tartrazine disrupts vascular formation both in zebrafish larvae and in human primary endothelial cells
- Type
- Study
- Evidence
- Animals and lab studies
- Summarised from
- Full text
- Cite
- Thanh DD, Bich-Ngoc N, Paques C, et al (2024). The food dye Tartrazine disrupts vascular formation both in zebrafish larvae and in human primary endothelial cells. Scientific reports. doi:10.1038/s41598-024-82076-5Free full textPubMed 39639097DOI
Summary written 26 Sep 2026. Check it against the paper before it changes what you eat. How we summarise papers · Report an error