A critical role for copper in aortic elastin structure and synthesis.

Abstract

Copper deficiency initiates extensive pathological changes in the major arteries of young chicks and pigs. These changes for the most part are localized within the elastic fibers in the vessel wall. Scanning electron micrographs of copper deficient chick aortas revealed randomly oriented fibrous ridges unevenly dispersed throughout the tunica media as well as structurally modified, stunted elastic fibers. A key role for copper in aorta is that of a cofactor for the enzyme lysyl oxidase. The enzyme catalyzes formation of desmosine and isodesmosine, and hence takes part in the polymerization of proelastin into mature elastic fibers. Besides serving as cofactor, copper may also regulate lysyl oxidase levels in aorta. Evidence supportive of this role has come from dietary studies where it was observed that chicks fed copper deficient diets suffered a rapid decline of lysyl oxidase activity. The enzyme activity was almost undetectable in aorta after 8 days — the time overt symptoms of the deficiency first appear. Returning copper to the diet restored complete enzymatic function.