Related Experiment Video
Updated: May 6, 2026

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC
Published on: May 10, 2016
Citrinin-Induced Cellular Damage: Insights from SH-SY5Y Cell Line Studies
Francisco J Martí-Quijal1,2, Felipe Franco-Campos2, Francisco J Barba1
1Research Group in Innovative Technologies for Sustainable Food (ALISOST), Nutrition, Food Science and Toxicology Department, Faculty of Pharmacy, Universitat de València, Avda. Vicent Andrés Estellés, s/n, 46100 Burjassot, València, Spain.
Citrinin (CIT), a mycotoxin in cereals, induces neurotoxicity by causing cell cycle arrest and apoptosis in human neuroblastoma cells (SH-SY5Y). Further research is needed to understand CIT
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Citrinin (CIT) is a mycotoxin found in cereals, produced by Aspergillus, Penicillium, and Monascus fungi.
- While CIT's nephrotoxicity is known, its neurotoxic effects are less understood.
- This study focuses on CIT's impact on human neuroblastoma cells (SH-SY5Y).
Purpose of the Study:
- To investigate the toxicity of Citrinin (CIT) in human neuroblastoma cells (SH-SY5Y).
- To determine the effects of CIT on cell cycle progression and apoptosis.
- To analyze changes in key apoptotic proteins following CIT exposure.
Main Methods:
- Cell viability was assessed using MTT and neutral red assays to determine IC50 values.
- Flow cytometry was used to analyze cell cycle distribution (G2/M and S phases).
- Western blot analysis was performed to examine the expression of apoptosis-related proteins (Bcl-2 and Bax).
Main Results:
- CIT exposure resulted in G2/M phase cell cycle arrest and increased S phase percentage in SH-SY5Y cells.
- Late apoptosis significantly increased in cells treated with higher concentrations of CIT.
- Western blot analysis showed rapid changes in the anti-apoptotic protein Bcl-2, with no significant alteration in Bax.
Conclusions:
- Citrinin induces apoptosis and cell cycle arrest in SH-SY5Y neuroblastoma cells.
- The findings suggest CIT activates cellular stress pathways.
- Further transcriptomic studies are required to elucidate the precise mechanisms of CIT neurotoxicity.

