mmpc-logo mmpc-logo
twitter-logo    bluesky-logo
| Create Account | login
Publication
Dioxin-like PCB 126 Increases Systemic Inflammation and Accelerates
Atherosclerosis in Lean LDL Receptor-Deficient Mice.
Authors Petriello MC, Brandon JA, Hoffman J, Wang C, Tripathi H, Abdel-Latif A, Ye X, Li
X, Yang L, Lee E, Soman S, Barney J, Wahlang B, Hennig B, Morris AJ
Submitted By Submitted Externally on 1/25/2019
Status Published
Journal Toxicological sciences : an official journal of the Society of Toxicology
Year 2018
Date Published 4/1/2018
Volume : Pages 162 : 548 - 558
PubMed Reference 29216392
Abstract Exposure to dioxins and related persistent organic pollutants likely contributes
to cardiovascular disease (CVD) risk through multiple mechanisms including the
induction of chronic inflammation. Epidemiological studies have shown that
leaner individuals may be more susceptible to the detrimental effects of
lipophilic toxicants because they lack large adipose tissue depots that can
accumulate and sequester these pollutants. This phenomenon complicates efforts
to study mechanisms of pollutant-accelerated atherosclerosis in experimental
animal models where high-fat feeding and adipose expansion limit the
bioavailability of lipophilic pollutants. Here, we investigated whether a model
dioxin-like pollutant, PCB 126, could increase inflammation and accelerate
atherosclerosis in Ldlr-/- mice fed a low-fat atherogenic diet. We fed Ldlr-/-
mice the Clinton/Cybulsky diet (10% kcal fat, 0.15% cholesterol) and sacrificed
mice at 8, 10, or 12 weeks postPCB (2 doses of 1 µmol/kg) or vehicle gavage. To
characterize this novel model, we examined the effects of PCB 126 on markers of
systemic inflammation, hematological indices, fatty livers, and atherosclerotic
lesion size. Mice exposed to PCB 126 exhibited significantly increased plasma
inflammatory cytokine levels, increased circulating biomarkers of CVD, altered
platelet, and red blood cell counts, increased accumulation of hepatic fatty
acids, and accelerated atherosclerotic lesion formation in the aortic root. PCB
126 also increased circulating neutrophils, monocytes, and macrophages as
determined by flow cytometry analysis. Exposure to dioxin-like PCB 126 increases
inflammation and accelerates atherosclerosis in mice. This low-fat atherogenic
diet may provide a useful tool to study the mechanisms linking exposure to
lipophilic pollutants to increased risk of CVD.




Menu

Home
Contact
About MMPC
Animal Husbandry
Tests Data
Search Data
Analysis
Clients
MMPC Centers

Newsletter

Interested in receiving MMPC News?
twitter-logo Mouse Phenotyping
@NationalMMPC



2017 National MMPC. All Rights Reserved.