Abstract
Even though the molecular mechanisms by which lead induces toxicity and cancer have been intensely studied for many years, its carcinogenic mechanisms are not well understood yet. Several possible mechanisms have been examined to gain understanding on the carcinogenic properties of lead, which include mitogenesis, alteration of gene expression, and oxidative damage, among others. The aim of the present study was to explore the induction of oxidative damage at low lead concentrations using human embryonic hepatic cells WRL-68. Our results showed induction of reactive oxygen species, changes in the superoxide dismutase and catalase activity, as well as an induction of lipidperoxidation and DNA damage. However, after 5 weeks of exposure, these alterations returned to their basal levels. These results taking together indicate that at low concentrations, lead is able to establish an oxidative stress scenario; however under optimal antioxidant defense the oxidative scenario could be abolished through an adaptative process.
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Acknowledgments
This study was supported by CONACyT project U44260-M, PHF and MS were the recipient of a fellowship from CONACyT. We want to thanks Dr. Veronica Monroy Martinez for her technical assistance in WRL-68 cell culture. Isabel Pérez Montfort corrected the English version of the manuscript. Authors report no conflicts of interest.
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Hernández-Franco, P., Silva, M., Valverde, M. et al. Induction of oxidative stress by low doses of lead in human hepatic cell line WRL-68. Biometals 24, 951–958 (2011). https://doi.org/10.1007/s10534-011-9453-2
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DOI: https://doi.org/10.1007/s10534-011-9453-2