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Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats
Journal article   Open access   Peer reviewed

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Hua Shen, Miao Li, Bingxuan Wang, Ian K Lai, Larry W Robertson and Gabriele Ludewig
Environmental science and pollution research international, Vol.21(10), pp.6384-6399
05/2014
DOI: 10.1007/s11356-013-1690-1
PMCID: PMC3769429
PMID: 23644946
url
http://doi.org/10.1007/s11356-013-1690-1View
Open Access

Abstract

Environmental pollutants polychlorinated biphenyls (PCBs), especially dioxin-like PCBs, cause oxidative stress and associated toxic effects, including cancer and possibly atherosclerosis. We previously reported that PCB 126, the most potent dioxin-like PCB congener, not only decreases antioxidants such as hepatic selenium (Se), Se-dependent glutathione peroxidase, and glutathione (GSH) but also increases levels of the antiatherosclerosis enzyme paraoxonase 1 (PON1) in liver and serum. To probe the interconnection of these three antioxidant systems, Se, GSH, and PON1, we examined the influence of varying levels of dietary Se and N-acetylcysteine (NAC), a scavenger of reactive oxygen species (ROS) and precursor for GSH synthesis, on PON1 in the absence and presence of PCB 126 exposure. Male Sprague-Dawley rats, fed diets with differing Se levels (0.02, 0.2, or 2 ppm) or NAC (1%), were treated with a single intraperitoneal injection of corn oil or various doses of PCB 126 and euthanized 2 weeks later. PCB 126 significantly increased liver PON1 mRNA, protein level and activity, and serum PON1 activity in all dietary groups but did not consistently increase thiobarbituric acid levels (thiobarbituric acid reactive substances, TBARS), an indicator of lipid oxidation and oxidative stress, in liver or serum. Inadequate (high or low) dietary Se decreased baseline and PCB 126-induced aryl hydrocarbon receptor (AhR) expression but further increased PCB 126-induced cytochrome P450 1A1 (CYP1A1) expression, the enzyme believed to be the cause for PCB 126-induced oxidative stress. In addition, a significant inverse relationship was observed not only between dietary Se levels and PON1 mRNA and PON1 activity but also with TBARS levels in the liver, suggesting significant antioxidant protection from dietary Se. NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 μmol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum. These results also show an unexpected predominantly inverse relationship between Se or NAC and PON1 during control and PCB 126 exposure conditions. These interactions should be further explored in the development of dietary protection regimens.
 Oxidation-Reduction Oxidative Stress Diet - statistics & numerical data Glutathione - metabolism Antioxidants - metabolism Liver - metabolism Acetylcysteine - metabolism Rats Male Thiobarbituric Acid Reactive Substances - metabolism Cytochrome P-450 CYP1A1 - metabolism Aryldialkylphosphatase - metabolism Rats, Sprague-Dawley Animals Selenium - metabolism Polychlorinated Biphenyls - toxicity Receptors, Aryl Hydrocarbon - metabolism Environmental Pollutants - toxicity ISRP Project 1 2015-2020

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