Biochemical reactions linked to atherosclerosis may harm other organs

April 12th, 2008 - 11:26 pm ICT by admin  

Washington, Apr 12 (ANI): Plaques formed during atherosclerosis, or hardening of the arteries have now been linked to some harmful biochemical reactions that may further lead to damage in the lungs, liver, and other organs, says a new study.

This breakthrough study has claimed that the effects of the disease are more widespread than previously believed, and may have implications in finding new targets for developing drugs for preventing or reducing these chemical changes associated with heart disease.

Our findings add new knowledge to the big melting pot of this complex disease called atherosclerosis. I anticipate that future research will establish whether the harmful protein modifications we observed in animal organs can be prevented and provide the basis of new treatments for the disease, said study leader Rita Upmacis, Ph.D., a chemist at Weill Medical College of Cornell University in New York.

In order to determine the root causes of the disease, the scientists focused on the interaction between certain highly reactive nitrogen molecules and proteins. Under certain conditions, this interaction produces nitrotyrosine, which has been linked to Alzheimers, arthritis, cancer, and other disorders, but little is known about its role in atherosclerosis.

In the new study, the scientists found that mice genetically prone to atherosclerosis and fed a high-fat diet, developed high levels of nitrotyrosine in their heart, lung, liver, and kidney, unlike mice that were fed regular diets.

The scientists said that the rise in nitrotyrosine levels indicate that high-fat diets in animals with atherosclerosis can help trigger nitrotyrosine accumulation in the proteins of various organs.

The team conducted a similar experiment in atherosclerotic mice lacking the gene that makes nitric oxide synthase (iNOS), an enzyme that orchestrates accumulation of nitrotyrosine in proteins. Supporting earlier finding that iNOS gene deletion limits the formation of atherosclerotic plaques; the new study showed that nitrotyrosine accumulation in proteins is reduced in diverse organs when iNOS is absent.

The findings support an emerging view that iNOS could be a new target for treating atherosclerosis and that limiting nitrotyrosine accumulation in the lungs, liver, and other organs could help fight the damaging effects of the disease. But the trick will be to develop a drug to block this pathway without causing any unwanted side effects, said Upmacis.

However, the scientists claim that the accumulation of nitrotyrosine in the blood can act as a diagnostic test to track atherosclerosis and give a clearer picture of damage to organs.

The study will be presented at the American Chemical Society national meeting in New Orleans . (ANI)

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