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Institute of Nutrition and Food Hygiene, Chinese Academy of Preventive Medicine, Beijing 100050, China * Division of Gastroenterology, Department of Medicine and Center in Molecular Toxicology, Vanderbilt University School of Medicine, Nashville, TN 37232
Selenium deficiency is necessary for the development of the cardiomyopathy known as Keshan disease. Healthy boys and men (1922 per group) from a low selenium area (Dechang County) and from an area where sodium selenite was added to salt (Mianning County) were studied. Keshan disease was endemic in Dechang but occurred rarely in Mianning. After an initial blood sampling, each subject received daily selenium supplements (100 µg selenium for boys and 200 µg for men) as sodium selenate for 14 d. Blood was sampled again at 7 and 14 d. Boys from Dechang had blood selenium levels similar to levels reported for patients with Keshan disease. Plasma glutathione peroxidase activity in boys and men from Dechang was 33 and 43%, respectively, of values from the corresponding groups in Mianning. Comparison of plasma selenium concentrations in boys and men from Dechang gave values of 33 and 38%, respectively, of the corresponding groups in Mianning. Selenium status did not affect red blood cell superoxide dismutase or catalase activities. Plasma vitamin E concentration was below the normal range in all groups but was unaffected by selenium status. Measurements of plasma malondialdehyde revealed no difference between subjects from Dechang and subjects from Mianning. Selenium supplementation raised plasma glutathione peroxidase activity and plasma selenium concentration in all groups. Groups with higher plasma selenium concentration had relatively smaller increases in glutathione peroxidase activity than in selenium concentration. These results characterize the selenium deficiency in subjects at risk for developing Keshan disease. The results obtained with supplementation of selenium indicate the presence of additional plasma forms of selenium besides glutathione peroxidase.
KEY WORDS: selenium humans Keshan disease blood selenium glutathione peroxidase selenium deficiency
1 Presented at the 73rd Annual Meeting of the Federation of American Societies for Experimental Biology held in New Orleans, LA, March 20, 1989, and published in abstract form: FASEB J. 3: A451, 1989.
2 Supported by National Institutes of Health grant HL 36371.
3 For a related article, see pp. 12361239 of this issue.
4 To whom reprint requests should be sent at C-2104, Medical Center North, Vanderbilt Medical Center, Nashville, TN 37232-2279.
Manuscript received 3 January 1989. Revision accepted 8 June 1989.
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