Roles of certain minerals, vitamin E and other factors in the genesis of myocardial fibrosis in mice.

Abstract

Thirty groups of inbred male C3H mice were studied in relation to the role of dietary minerals and other nutrients in the induction of myocardial damage. It has been found that a level of vitamin E in the diet which was adequate in the presence of ferric phosphate was not adequate in the presence of ferrous sulfate, and became more inadequate when the trace minerals, Co, Cu, Mn, Zn and I were added in amounts provided in the Jones-Foster salt formula. These variables are of critical importance in the development of heart lesions. Reduction of the cod liver oil content of the diet did not prevent the myocardial damage although there was a progressive decline in frequency and increase in the age at onset of the heart failure as the level of the cod liver oil varied from 2, to 1, and to 0%. The incidence of such diet-induced myocardial damage could be greatly reduced by caloric restriction alone. In the absence of vitamin E caloric restriction only delays the onset of myocardial damage. The heart-body weight ratio is increased in mice with myocardial damage as is the water content of the heart. Additions of vitamin E, orally or parenterally at 350 days of age, did not markedly protect mice against later development of the disorder. The age at onset may have been increased by such treatment.