Abstract
Oxidative damage of DNA and lipids in normal primary rat hepatocyte cultures and in hepatoma Fao cell-line was induced by ferric nitrilotriacetate (Fe-NTA). DNA oxidation was evidenced by measuring the mutagenic oxidized nucleoside 8-hydroxy-2′-deoxyguanosine (8-oxodG). An increase in 8-oxodG production was induced by Fe-NTA in the two different cell cultures. Moreover, this increase was more important in hepatocytes than in Fao cells. In addition, the extent of lipid peroxidation was higher in normal hepatocytes than in Fao cells. These observations demonstrated a higher resistance of tumor cells than normal hepatocytes to oxidative stress. Since DNA lesions induced by oxidative stress are now recognized as being involved in the mutagenesis process and since normal hepatocytes appeared particularly sensitive to iron-induced oxidative damage, a high level of iron should be considered as a potent toxic factor involved in normal cell degeneration. This findings might partly explain the propensity of hepatic iron-overload diseases for cancerous evolution.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.