Oral exposure to acrolein exacerbates atherosclerosis in apoE-null mice

Abstract

Background-Acrolein is a dietary aldehyde that is present in high concentrations in alcoholic beverages and foods including cheese, donuts and coffee. It is also abundant in tobacco smoke, automobile exhaust and industrial waste and is generated in vivo during inflammation and oxidative stress.Objectives-The goal of this study was to examine the effects of dietary acrolein on atherosclerosis.Methods-Eight-week old male apoE-null mice were gavage-fed acrolein (2.5 mg/kg/day) for 8 weeks. Atherosclerotic lesion formation and composition and plasma lipids and platelet factor 4 (PF4) levels were measured. Effects of acrolein and PF4 on endothelial cell function was measured in vitro.Results-Acrolein feeding increased the concentration of cholesterol in the plasma. NMR analysis of the lipoproteins showed that acrolein feeding increased the abundance of small and medium VLDL particles. Acrolein feeding also increased atherosclerotic lesion formation in the aortic valve and the aortic arch. Immunohistochemical analysis showed increased macrophage accumulation in the lesions of acrolein-fed mice. Plasma PF4 levels and accumulation of PF4 in atherosclerotic lesions was increased in the acrolein-fed mice. Incubation of endothelial cells with the plasma of acrolein-fed mice augmented transmigration of monocytic cells, which was abolished by anti-PF4 antibody treatment.Conclusions-Dietary exposure to acrolein exacerbates atherosclerosis in apoE-null mice. Consumption of foods and beverages rich in unsaturated aldehydes such as acrolein may be a contributing factor to the progression of atherosclerotic lesions.

Augmented atherogenesis in ApoE-null mice co-exposed to polychlorinated biphenyls and 2,3,7,8-tetrachlorodibenzo-p-dioxin

“…Because of the extensive disposition and coexistence of these persistent organic pollutants in the environment, it is important to study the mixture effects of multiple pollutants. Furthermore, the interplay of multiple factors including hyperlipidemia, endothelial activation, monocyte recruitment and differentiation into macrophages, foam cell formation and activation of platelets is well documented in the pathogenesis of atherosclerosis (Srivastava et al, 2011;Cheng et al, 2013;Li, 2013). Our study demonstrated that combined exposure to Aroclor1254 and TCDD clearly exacerbated the enhancement of atherosclerosis induction as evidenced by much more severe injuries in the aortic valve and aortic arch than under individual exposures.…”

“…PF4 has been shown to be atherogenic, and the PF4 gene knockout has been shown to diminish atherosclerotic lesion formation in ApoE −/− mice (Sachais et al, 2007;Srivastava et al, 2011). Therefore, we examined PF4 expression in the atherosclerotic lesions of mice receiving Aroclor1254 and TCDD alone or in combination (Figs.…”

Atherogenesis and metabolic dysregulation in LDL receptor–knockout rats

“…Cholesterol distribution in the lipoproteins was assessed by size-exclusion chromatography on FPLC (62). Particle size of lipoproteins was measured by NMR as described (64).…”

“…Total protein, albumin, ALT, AST, creatinine, CK, and NEFA in the plasma were measured on MIRA chemical analyzer as described (64).…”

Efeito dos resíduos de café seco e fermentado por Monascus ruber no metabolismo de camundongos Apo E

“…Several studies have shown that a high-calorie ingestion and consumption of diets rich in saturated fatty acids accelerate atherogenesis; however, the effects of the dietary individual components are still little understood 6 .…”