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    Mechanisms underlying citrinin-induced toxicity via oxidative stress and apoptosis-mediated by mitochondrial-dependent pathway in SH-SY5Y cells
    (Taylor and Francis Ltd., 2022) Abudayyak, Mahmoud; Karaman, Ecem Fatma; Ozden, Sibel
    Citrinin (CIT) is a mycotoxin produced as a secondary product by the generaAspergillus,Penicillium,Monascus,and other strains. CIT has the potential for contaminating animal feed and human food suchas maize, wheat, rye, barley, oats, rice, cheese, and sake. Although CIT is primarily known as a nephro-toxic mycotoxin, it also affects other organs, including the liver and bone marrow, and its mechanisms oftoxicity have not been clearly elucidated. There is a further lack of studies investigating the potential forCIT-induced neurotoxicity and its mechanisms. In the current study, SH-SY5Y human neuroblastoma cellline was treated with CIT for 24 h to evaluate various toxicological endpoints, such as reactive oxygenspecies (ROS) production and apoptosis induction. Results indicate that CIT has an IC50value of250.90lM and cell proliferation decreased significantly at 50 and 100lM CIT concentrations. These sameconcentrations also caused elevated ROS production ( 34.76%), apoptosis ( 9.43-fold) and calcium ionmobilization ( 36.52%) in the cells. Results show a significant decrease in the mitochondrial membranepotential ( 86.8%). We also found that CIT significantly upregulated the expression of some genesrelated to oxidative stress and apoptosis, while downregulating others. These results suggest that apop-tosis and oxidative stress may be involved in the mechanisms underlying CIT-induced neurotoxicity.