Selenium in Chronic Neurologic Diseases
The selenium levels in whole blood and the activity of glutathione peroxidase in hematogenous cells of normal Danes have been defined taking into account sex and confounding factors such as smoking and aging. No differences related to sex could be found with regard to the selenium level, and peroxidase activity assayed with hydrogen peroxide. However, the peroxidase activity assayed with t-butyl hydroperoxide was higher in females than in males (p < .05). The peroxidase activities are dependent on age. Thus, the peroxidase levels assayed with both substrates show a minimum value in the age group from 40 to 50 yr for both smokers and nonsmokers. Smokers did show more homogeneous values as a function of age than non-smokers. Smokers had significantly lower selenium values than non-smokers, but glutathione peroxidase values identical with those of nonsmokers. Multiple sclerosis (MS) patients suffer from a chronic relapsing/remitting demyelinating disease. A theory explaining the pathogenesis of MS concerns increased stickiness of cellular plasma membranes, hampering normal vascular function of the brain. In agreement with that theory, the present communication demonstrates significantly lowered selenium values and lowered glutathione peroxidase activities of major types of hematogenous cells. In close agreement with these findings, hematogenous cells in MS show increased peroxidation rates. A nonblinded biochemical dietary experiment on MS patients showed that all abnormalities could be normalized by daily intake of selenium, vitamin E, and vitamin C.
Batten’s disease is a recessive inherited neurodegenerative disorder clinically characterized by progressive loss of vision, epilepsy, and dementia. Neuropathologically, this disease is characterized by storage of lipofuscin in nervous tissue. We have in a few cases documented a low selenium status and low glutathione peroxidase activities of hematogenous cells. As in MS, we normalized the biochemical abnormalities by an antioxidative treatment. Like in similar Finnish studies, the biochemical parameters can be normalized. Further, the Finnish studies indicate it possible by an antioxidative treatment to inhibit progression of the mental deterioration.
The data presented will be discussed in relationship both to specific pathological parameters of the diseases and to the low dietary energy expenditures of handicapped immobile patients.
Index EntriesSelenium, in chronic neurologic diseases selenium, in multiple sclerosis selenium, in Batten’s disease
Unable to display preview. Download preview PDF.
- 1.J. Clausen, and J. Jensen, Ugeskr.f.Laeger 37, 2155–2162, 1975Google Scholar
- 2.B. Borgstrom, I. Dencker, and Å. Norden, Lækartidn. 67, 3678, 1970.Google Scholar
- 4.C. F. Combs, and S. B. Combs, Ann. Rev. BioChem. 4, 257–280, 1984.Google Scholar
- 5.H. Mickel, Perspectives Biol. Med. 18, 363–374 (1975).Google Scholar
- 6.R. H. S. Thompson, Biochem. Soc. Symp. no 35, Ganguly, J. and Smellie, eds., Academic, London, 1972.Google Scholar
- 7.G. E. Jensen and J. Clausen, Glutathione Peroxidase activities in leukocytes, erythrocytes and serum from juvenile form of neuronal lipofuscinosis, in Ceroid-lipofuscinosis (Batten’s disease), Armstrong, D., Koppang, N., and Rider, J. A., eds., 1982.Google Scholar
- 9.L. S. Wolfe, Ng, N. M. K., Y. Kin, and R. R. Baker, Batten’s disease and related disorders: New findings on the chemistry of the storage material, in, Lysosomes and lysosomal storage diseases, Callahan, J. W. and Lowden, J. A., eds., Raven, New York, 1981, pp. 311–330.Google Scholar
- 14.D. E. Paglia, and W. N. Valentine, J. Lab. Clin. Med. 70, 158, 1970.Google Scholar
- 22.C. Clark, L. Fed. Proc. 44, 258–2589, 1985.Google Scholar
- 28.L. J. Galland, Am. Coll. Nutr. 5, 213–228, 1986.Google Scholar
- 29.J. M. Bailey, R. W. Bryant, C. E. Low, M. B. Pupillo, and J. Y. Vanderhoek, Role of Lipoxygenase in Regulation of PHA and Phorbol Ester-Induced Mitogenesis: Leucotrienes and Other Lipoxygenase Products, B. Samuelsson, ed., Raven, New York, 1982, pp. 341–353.Google Scholar
- 30.A. S. Csallany, L.-C. Su, Scientif. J. Series Minnesota Agricultural Exp. Station paper no. 55108, 1984.Google Scholar
- 33.G. N. Schrauzer, J. E. McGinness, and K. Kuehn, Caronogenesis (London), 1, 199–201, 1980.Google Scholar
- 34.J. Clausen and J. Moller, Internat. Arch Allergy 36, 224–233, 1969.Google Scholar
- 36.J. Miquel, K. G. Bensch, and J. E. Johnson, Lipofuscinosis: Fine structural and biochemical studies, in, Radicals in Biology, Pryor, W. A., ed., Academic, New York, 1977, pp. 133–182.Google Scholar