Effects of selenium deficiency on the rat myocardial protein pattern - investigation by two-dimensional gel electrophoresis

Dietary selenium deficiency represents an etiological factor in "Keshan dis ease", a distinct form of an endemic cardiomyopathy. The biochemical effect s of selenium depletion in the myocardium are, however, not yet known. Ther efore, we investigated the changes in the myocardial protein pattern in rat s after long-term selenium deficiency. The myocardial proteins were analyzed in samples from five selenium-deplete d rats (Se-deficient group) and five rats supplied with adequate amounts of the element (Se-adequate group). Isoelectric focusing (IEF) with carrier a mpholytes on large 2-DE gels was used for the separation of proteins in the first dimension and sodium dodecyl sulfate-polyacrylamide gel electrophore sis (SDS-PAGE) for the second dimension. The protein patterns were evaluate d by means of a computer-assisted gel analysis system. The biochemical iden tification of the proteins of interest was achieved by matrix-assisted lase r desorption/ionization mass spectrometry (MALDI) or immunoblotting. On average, 588 +/- 68 protein spots were found on the gels. No significant difference in spot numbers existed between the groups. A pattern of 270 sp ots with identical positions was found on every gel; 247 of these spots wer e not saturated and used for quantitative comparison. Thirty-five, i.e., 14 %, differed significantly in their relative intensity in the two groups. Tw enty-eight protein spots were decreased in the Se-deficient group and seven were increased. Sarcomeric creatine kinase M chain, ol-myosin heavy chain (alpha-MHC) and myosin light chain 1 and 2 (MLC 1 and 2) were largely decre ased in Se-deficiency. Three protein spots were increased by more than twof old or appeared only in the Se-deficient group. A mitochondrial creatine ki nase was identified in this group. The results suggest that selenium deficiency affects myocardial energy meta bolism and contractile proteins. These changes probably reflect non-specifi c alterations in heart failure.