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. 2005 Jan;113(1):83-7.
doi: 10.1289/ehp.7280.

Dietary fat interacts with PCBs to induce changes in lipid metabolism in mice deficient in low-density lipoprotein receptor

Bernhard Hennig  1 , Gudrun Reiterer, Michal Toborek, Sergey V Matveev, Alan Daugherty, Eric Smart, Larry W Robertson
Affiliations

Dietary fat interacts with PCBs to induce changes in lipid metabolism in mice deficient in low-density lipoprotein receptor

Bernhard Hennig et al. Environ Health Perspect. 2005 Jan.

Abstract

There is evidence that dietary fat can modify the cytotoxicity of polychlorinated biphenyls (PCBs) and that coplanar PCBs can induce inflammatory processes critical in the pathology of vascular diseases. To test the hypothesis that the interaction of PCBs with dietary fat is dependent on the type of fat, low-density lipoprotein receptor-deficient (LDL-R(-/-)) mice were fed diets enriched with either olive oil or corn oil for 4 weeks. Half of the animals from each group were injected with PCB-77. Vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arches was nondetectable in the olive-oil-fed mice but was highly expressed in the presence of PCB-77. PCB treatment increased liver neutral lipids and decreased serum fatty acid levels only in mice fed the corn-oil-enriched diet. PCB treatment increased mRNA expression of genes involved in inflammation, apoptosis, and oxidative stress in all mice. Upon PCB treatment, mice in both olive- and corn-oil-diet groups showed induction of genes involved in fatty acid degradation but with up-regulation of different key enzymes. Genes involved in fatty acid synthesis were reduced only upon PCB treatment in corn-oil-fed mice, whereas lipid transport/export genes were altered in olive-oil-fed mice. These data suggest that dietary fat can modify changes in lipid metabolism induced by PCBs in serum and tissues. These findings have implications for understanding the interactions of nutrients with environmental contaminants on the pathology of inflammatory diseases such as atherosclerosis.

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Figures

Figure 1
Figure 1. Fatty acid analysis of the two oils used in the feeding study. Fatty acids are measured in g/100 g total fatty acids; palmitic acid, 16:0; stearic acid, 18:0; oleic acid, 18:1; linoleic acid, 18:2; arachidonic acid, 20:4.
Figure 2
Figure 2. Fatty acid profile in serum. See “Materials and Methods” for details. Values are mean ± SEM (n = 5). Palmitic acid, 16:0; stearic acid, 18:0; oleic acid, 18:1; linoleic acid, 18:2; arachidonic acid, 20:4. : *Significantly different from respective diet treatment without PCBs.
Figure 3
Figure 3. Lipid staining of mouse liver sections. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Magnification, 200×.
Figure 4
Figure 4. Immunoreactivity of VCAM-1 antiserum against sections of mouse aortic arches. (A) Olive oil. (B) Olive oil plus PCB. (C) Corn oil. (D) Corn oil plus PCB. See “Materials and Methods” for details. Red staining reflects positive chromogen development for VCAM-1 immunostaining on the endothelial surface (B–D) and in subendothelial tissue (D). Magnification, 400×.
Figure 5
Figure 5. mRNA expression of acetyl-CoA-carboxylase (A) and CYP1A1 (B) as analyzed by RT-PCR; gels below show one representative sample per treatment group of RT-PCR. Abbreviations: CO, corn oil; OO, olive oil. See “Materials and Methods” for details. Values are mean ± SEM (n = 5); values are normalized to β-actin. : *Significantly different from all other groups, p < 0.05.
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