Zinc deficiency induces vascular pro-inflammatory parameters associated with NF-kappaB and PPAR signaling.

Objectives: Marginal intake of dietary zinc can be associated with increased risk of cardiovascular diseases. In the current study we hypothesized that vascular dysfunction and associated inflammatory events are activated during a zinc deficient state.

Design: We tested this hypothesis using both vascular endothelial cells and mice lacking the functional LDL-receptor gene.

Benzo[a]pyrene induces intercellular adhesion molecule-1 through a caveolae and aryl hydrocarbon receptor mediated pathway.

Toxicologic and epidemiologic studies have linked benzo[a]pyrene (B[a]P) exposure with cardiovascular diseases such as atherosclerosis. The mechanisms of action leading to these diseases have not been fully understood. One key step in the development of atherosclerosis is vascular endothelial dysfunction, which is characterized by increased adhesiveness.

Alumina nanoparticles induce expression of endothelial cell adhesion molecules.

Nanotechnology is a rapidly growing industry that has elicited much concern because of the lack of available toxicity data. Exposure to ultrafine particles may be a risk for the development of vascular diseases due to dysfunction of the vascular endothelium. Increased endothelial adhesiveness is a critical first step in the development of vascular diseases, such as atherosclerosis.

Impact of nutrition on PCB toxicity.

Studies are evolving which suggest that nutritional intervention can modify pathologies of diseases associated with environmental toxic insults. The diet is a major route of exposure to environmental toxins, such as persistent organic pollutants and heavy metals. Many persistent organics, such as polychlorinated biphenyls (PCBs), bioaccumulate in our bodies and "bioremediation" is extremely difficult.

Renin inhibition reduces hypercholesterolemia-induced atherosclerosis in mice.

The role of the renin angiotensin system (RAS) in atherosclerosis is complex because of the involvement of multiple peptides and receptors. Renin is the rate-limiting enzyme in the production of all angiotensin peptides. To determine the effects of renin inhibition on atherosclerosis, we administered the novel renin inhibitor aliskiren over a broad dose range to fat-fed LDL receptor-deficient (Ldlr(-/-)) mice.

Environmental toxicity, nutrition, and gene interactions in the development of atherosclerosis.

There is substantial evidence from epidemiological studies that the pathology of cardiovascular diseases is linked in part to environmental pollution. Many environmental contaminants, and especially persistent organic pollutants, are risk factors for atherosclerosis because they may exacerbate an underlying disease by altering gene expression patterns. Many mechanisms and signaling pathways associated with the pathology of "modern" diseases are similarly modulated by poor dietary habits and environmental pollutants.

Modification of environmental toxicity by nutrients: implications in atherosclerosis.

We hypothesize that nutrition can modulate the toxicity of environmental pollutants and thus modulate health and disease outcome associated with chemical insult. There is now increasing evidence that exposure to persistent organic pollutants, such as PCBs, can contribute to the development of inflammatory diseases such as atherosclerosis. Activation, chronic inflammation, and dysfunction of the vascular endothelium are critical events in the initiation and acceleration of atherosclerotic lesion formation.