Se Deficiency Is a Necessary But Not Sufficient Factor Required for the Pathogenesis of Keshan Disease.

Abstract

The experimental results obtained from rats and guinea pigs fed a semisynthetic diet low in Se indicated no obvious changes in ultrastructure and oxidative phosphorylation of mitochondrial membranes. But the animals fed cereals from Keshan disease(KD)-endemic areas appeared to have significant abnormalities in ultrastructure and energy transduction of myocardial mitochondria: electron microscopy showed swelling of mitochondria in which the cristae were arranged in disorderly fashion and the mitochondrial membranes were less clear or even absent, the activities of succinic oxidase and cytochrome c oxidase were remarkably decreased, and the oligomycin sensitivity of H+-ATPase had a tendency to decline. However, when the diet from the KD area was supplemented with Se, all the abnormalities mentioned above were reduced significantly. The Se content of mitochondria of the animals fed either the semisynthetic diet low in Se or the diet from the KD area was lower, with statistical significance, than that of animals fed the normal diet. Supplementation of Se to the diet from KD area resulted in an increase in the Se content of mitochondria to the normal level. From the fact that the semisynthetic diet with low Se has no harmful effect on the ultrastructure and function of myocardial mitochondria it can be deduced that Se deficiency alone can not induce severe heart damage in experimental animals. Presumably, other factors in addition to Se deficiency are required for the pathogenesis of KD.