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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Ochratoxin A (OTA) and citrinin (CIT) are nephrotoxic mycotoxins commonly found in contaminated agricultural products. Exposure to both mycotoxins has been associated with Balkan Endemic Nephropathy (BEN), a disease marked by interstitial renal fibrosis. Their mechanism of toxicity is unclear; however, they are known for promoting oxidative damage via the production of reactive oxygen species (ROS), warranting the need for further investigation and protective strategies. This study aimed to evaluate the protective effect of 5-hydroxy-1-methylhydantoin (NZ-419), a creatinine metabolite with hydroxyl radical scavenging properties, against OTA- and CIT-induced toxicity in human kidney (HK-2) cells.
HK-2 cells were seeded at a density of 1 × 10⁵ cells/well, incubated overnight, and then exposed to OTA or CIT in the presence of NZ-419 for 24 hours. The effects of NZ-419 on OTA- or CIT-induced cytotoxicity, oxidative stress, and mitochondrial membrane potential (MMP) were assessed. To evaluate whether NZ-419 alters the expression of proteins related to oxidative stress, apoptosis, and fibrosis, HK-2 cells were exposed to OTA or CIT in the presence of NZ-419 for 6 hours, followed by protein extraction and Western blot analysis. The expression of antioxidant-related genes was evaluated using quantitative PCR. To assess the effect of NZ-419 on HK-2 cells under hypoxic conditions, cells were incubated under normoxic or hypoxic conditions using the AnaeroPack system, and ROS, MMP and fibrosis-related proteins were evaluated.
Both OTA and CIT exhibited dose-dependent cytotoxicity with IC50 values of 195.0 nM and 56.6 µM (p < 0.01), respectively. Treatment with NZ-419 (10 µM-1 mM) showed significant cytoprotective effects against OTA-induced cytotoxicity (p < 0.05) but had no significant effect against CIT (p ˃ 0.05). Nevertheless, NZ-419 (1 mM) suppressed OTA- and CIT-induced ROS, malondialdehyde (MDA), and NADPH oxidase (NOX4). It further activated the Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway and upregulated the expression of antioxidant genes such as superoxide dismutase 1 (SOD1), glutathione peroxidase (GPx), and catalase (CAT). It also exhibited anti-apoptotic effects by improving MMP and increasing B-cell lymphoma 2 (Bcl-2) levels. Furthermore, it inhibited hypoxia-inducible factor 1-alpha (HIF-1α) and connective tissue growth factor (CTGF) levels, key mediators of renal fibrosis.
NZ-419 protects against mycotoxin-induced oxidative stress and cellular injury by enhancing antioxidant defenses and reducing fibrosis-related signaling. These findings suggest NZ-419 as a promising candidate for mitigating nephrotoxicity associated with dietary mycotoxin exposure.
