Please use this identifier to cite or link to this item:
|Title:||Expression of major HDL-associated antioxidant PON-1 is gender dependent and regulated during inflammation||Authors:||Ali, A.B.
|Issue Date:||1-Apr-2003||Citation:||Ali, A.B., Zhang, Q., Lim, Y.K., DONG FANG, Retnam, L., Lim, S.-K. (2003-04-01). Expression of major HDL-associated antioxidant PON-1 is gender dependent and regulated during inflammation. Free Radical Biology and Medicine 34 (7) : 824-829. ScholarBank@NUS Repository. https://doi.org/10.1016/S0891-5849(02)01436-3||Abstract:||Paraoxonase 1, an HDL-associated enzyme that confers antioxidant activity on HDL, and its activity in serum have been correlated with protection against atherosclerosis, an oxidative disease. However, serum PON-1 activity is highly variable and its regulation is complex, involving both genetic and environmental factors. It is influenced by gender and inflammation, two important factors in atherosclerosis. Serum PON-1 activity has been shown to be lower in male mice and is decreased in male Syrian hamster during inflammation. Here we show that male mice had lower hepatic PON-1 mRNA that increased by 170% after castration. Our data also suggested that this effect was testes but not plasma testosterone dependent. Ovariectomy had no effect on PON-1 mRNA in female mice. LPS caused hepatic PON-1 mRNA to decrease further in male mice, and to increase moderately in female mice. Anti-inflammatory dexamethasone enhanced PON-1 mRNA level by 2-fold in male and female LPS-treated mice, and increased PON-1 expression by 8-fold in Hepa cell, a mouse hepatoma cell line. Therefore, antioxidant PON-1 is regulated at the mRNA level in a gender-specific manner by proinflammatory LPS and anti-inflammatory dexamethasone. © 2003 Elsevier Science Inc.||Source Title:||Free Radical Biology and Medicine||URI:||http://scholarbank.nus.edu.sg/handle/10635/53430||ISSN:||08915849||DOI:||10.1016/S0891-5849(02)01436-3|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.