Heavy metals and hardened arteries

The way in which arterial plaques form, atherogenesis, is not yet completely understood despite a significant number of research studies in this area. Now, a study using rabbits on a high-fat diet (HFD) has investigated the effects of changes in the concentrations of trace elements., iron (Fe), copper (Cu) and zinc (Zn), in several tissues using atomic absorption spectroscopy.

Atherosclerosis, or arteriosclerotic vascular disease , is commonly known as "hardening", or "furring" of the arteries. It is a condition in which the artery wall becomes thicker as fatty material, such as cholesterol, is deposited on the inner surface, narrowing the artery and stymieing blood flow. It is a chronic inflammatory condition within the arteries largely due to the accumulation of macrophage white blood cells and promoted by low-density lipoproteins. These are the plasma proteins that carry cholesterol and triglycerides in the blood. For some reason adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL) fails and leads to multiple plaques within the arteries.

Mohamed Anwar Abdelhalim and Hisham Alhadlaq of the College of Science, King Saud University and Sherif Abdelmottaleb Moussa of the King Khalid Military College, Saudi Arabia have endeavoured to unravel one aspect of atherogenesis using 20 white male rabbits.

The team fed rabbits in the HFD group an NOR rabbit chow supplemented with 1.0% cholesterol plus 1.0% olive oil. The researchers measured Fe, Cu and Zn concentrations in four different types of tissue from control and HFD rabbits using AAS. Tissue samples were wet digested with nitric acid and converted into acidic digest solution, which were freeze dried in order to minimize loss of analytes and to facilitate subsequent sample preparation steps, and then homogenized to a fine powder by ball-milling in plastic containers for AAS analysis.

When they compared HFD rabbits to control rabbits, they found that the highest percentage change of increase of iron was 95% in lung tissue, while the lowest percentage change of increase of iron was 7% in kidney tissue. Copper decreased by 16% in aortic tissue, but by only 6% in kidney tissue. Zinc levels fell by 71% in kidney tissue, but just 8% in lung tissue. "These results suggest that Fe plays a major role in atherogenesis," the teams says.

They hypothesise that the presence of iron may accelerate the process of atherosclerosis through a variety of processes, not least the production of free radicals. They also suggest that iron may lead to deposition and absorption of intracellular and extracellular lipids in the intima, connective tissue formation, smooth muscle proliferation, lower matrix degradation capacity and increased plaque stability. One further piece of evidence for the role of iron in atherogenesis, is that anaemia in HFD rabbits delayed or inhibited the progression of atherosclerosis.

They add that copper plays only a minor role in atherogenesis, although dietary supplementation with copper may inhibit the progression of atherogenesis by reducing the migration of smooth muscle cells from the media to the intima. Zinc too may have a small role in that it can act as an endogenous protective factor by reducing the iron content of lesions, reducing intracellular and extracellular lipids in the intima, connective tissue formation, and smooth muscle proliferation. "It [is] evident from this study that the changes in trace elements would alter the initiation and progression of atherosclerosis in HFD rabbits," the team says.

"These results suggest that it may be possible to use the measurement of changes in trace elements in different tissues of rabbits as an important risk factor during the progression of atherosclerosis," the team concludes. How the results might translate to other mammals and humans will, of course, be the subject of further studies.