Arda Oğuz AYGÖRDÜ, Alper BÜKREK, Seher SALCI, Buse Elif KÜRÇE, Hande YÜCE, Dilan AŞKIN ÖZEK, Songül ÜNÜVAR
Anatolian Journal of Pharmaceutical Sciences - 2026;5(1):8-17
Citrinin (CIT) is a mycotoxin commonly found in foods and has been linked to toxicity in various cell types. In our study, we investigated the effect of CIT on human lung adenocarcinoma (A549), colorectal cancer (HCT-116), and healthy fibroblast (L929) cells, used as a control. MTS-based evaluation of cell viability demonstrated that CIT reduced cell viability in a manner dependent on both dose and exposure time. Interestingly, HCT-116 cells were more sensitive to CIT than A549 cells, suggesting that its effects can vary between cancer types. We also performed wound healing experiments to assess wound closure and proliferation. CIT significantly slowed these processes in cancer cells, while fibroblasts were less affected. These results suggest that CIT can inhibit the spread of cancer cells, although it also affects normal cells. Previous studies have proposed several mechanisms for CIT's toxicity. It appears to promote apoptosis by generating reactive oxygen species, disrupting mitochondrial membrane potential, activating caspases, and inducing endoplasmic reticulum stress. While CIT exhibited cytotoxic and antimigratory effects in cancer cell lines, its high toxicity in the normal L929 fibroblast line and limited selectivity represent major limitations for therapeutic consideration. Overall, our findings highlight that CIT's biological effects are cell-line-specific, underscoring the need for further studies to determine conditions or doses that could enhance tumor-selective activity while reducing harm to healthy cells.
