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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/32735
Title: Lead inhibits paraoxonase 2 but not paraoxonase 1 activity in human hepatoma HepG2 cells
Authors: Wanida Sukketsiri
Sureerut Porntadavity
Laddawal Phivthong-ngam
Somsong Lawanprasert
Chulalongkorn University
Mahidol University
Srinakharinwirot University
Keywords: Pharmacology, Toxicology and Pharmaceutics
Issue Date: 1-Jul-2013
Citation: Journal of Applied Toxicology. Vol.33, No.7 (2013), 631-637
Abstract: Lead is an environmental toxicant of great concern for humans and animals. Lead-induced liver damage and malfunction are partly due to a disturbance of the cellular antioxidant balance. Paraoxonase 1 (PON1) and PON2 are highly expressed in the liver and have been proposed as antioxidative enzymes. In this study, the effects of lead on PON1 and PON2 activities were investigated in human hepatoma HepG2 cells by exposing the cells to various concentrations of lead acetate for 24, 48, or 72h. The results show that a significant increase in reactive oxygen species was observed even at the lowest concentration of lead treatment. However, only the highest concentration of lead significantly influenced cell viability. Lead had no influence on cell-associated PON1 activity, but it significantly decreased cytoplasmic PON2 activity in a concentration- and time-dependent manner. This reduction was rescued by the addition of calcium. A significant increase of PON2 transcript was observed by real-time polymerase chain reaction, while PON2 protein expression did not change in the western blot analysis. Taken together, these results indicate that lead reduces PON2, but not PON1, activity and that this reduction is reversed by calcium. Lead-induced oxidative stress and decreased PON2 activity lead to the upregulation of PON2 transcript. © 2012 John Wiley & Sons, Ltd.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84878193221&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/32735
ISSN: 10991263
0260437X
Appears in Collections:Scopus 2011-2015

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