Abstract
This study aimed to investigate the in vitro damage induced by ochratoxin A (OTA) in BME-UV1 and MDCK epithelial cells. Both cells lines were treated with OTA (0 up to 10μg/mL), and cell viability (MTT assay), membrane stability (lactate dehydrogenase (LDH) release assay) and apoptotic cell rate (Tunel assay) were investigated. Further, the effect of the incubation with OTA has been evaluated at DNA level by the determination of DNA integrity, by the quantification of DNA adduct formation (8-hydroxy-2'-deoxyguanosine (8-OHdG)) and by the assessment of the global DNA methylation status (5-methyl-cytosine (5-mC)). The obtained results showed that after 24h of OTA treatment, BME-UV1 cell viability was reduced in a dose-dependent way. OTA significantly (P < 0.05) increased LDH release in BME-UV1 cells at all concentrations tested. OTA (1.25μg/mL) induced 35% LDH release in MDCK cells (P < 0.05). A significant (P < 0.05) change in percentages of apoptotic BME-UV1 (10 ± 0.86) and MDCK (25 ± 0.88) cells was calculated when the cells were co-incubated with OTA. The level of 8-OHdG adduct formation was significantly (P < 0.05) increased in BME-UV1 cells treated with 1.25μg/mL of OTA. The results of the present study suggest that a different mechanism of action may occur in these cell lines. Graphical abstract Study results overview.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
