Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract only
Publication Acceptance Date: 4/6/1997
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: DHEA is a metabolic precursor of testosterone implicated by some in the progression of coronary atherosclerosis and the aging process. Because DHEA synthesis requires oxidative transformation of cholesterol we decided to test the hypothesis that copper deficiency can decrease DHEA in serum. Male, weanling rats of the Sprague-Dawley strain were matched into equal groups by mean weight (49.8g) and were fed a purified diet (Klevay, Am J Clin Nutr 26:1060, 1973) based on corn oil (10%), egg white protein (20%) and sucrose (62%). All rats drank water with 10 ug zinc/ml (as acetate); water for supplemented rats also contained 3 ug copper/ml (as sulfate). When hypercholesterolemia was detected after 35 days by fluorometry (mean +/- SE) (135 mg/dl +/- 7.4 vs. 114 +/- 6.4, p<0.05) and two deficient rats had died with atrial thrombosis, DHEA and its sulfate (DHEAS) were measured in serum by a commercial immunoassay. Because of positive skewness, the first statistical comparison was by the Wilcoxon two-sampl test (p<0.04) for n=18 with deficient and supplemented median values of 0.60 ng/ml and 1.17, respectively. Then, removal of one value in each group which was more than two SD from the mean resulted in mean values of 0.55 ng/ml +/- 0.08 and 1.18 +/- 0.19, for deficient and supplemented groups, respectively (p<0.02 by "t" test for unequal variances). Significant change in DHEAS was not found; values seemed higher in deficiency. Copper deficiency can modify DHEA metabolism. As diets in the United States often are low in copper, physiological consequences of these observations should be explored.