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. 1977 Aug;19:159–164. doi: 10.1289/ehp.7719159

Metabolic interrelationships between arsenic and selenium

Orville A Levander
PMCID: PMC1637401  PMID: 332496

Abstract

In 1938, Moxon discovered that arsenic protected against selenium toxicity. Since that time it has been shown that this protective effect of arsenic against selenium poisoning can be demonstrated in many different animal species under a wide variety of conditions. Antagonistic effects between arsenic and selenium have also been noted in teratologic experiments.

Early metabolic studies showed that arsenic inhibited the expiration of volatile selenium compounds by rats injected with acutely toxic doses of both elements. This was puzzling since pulmonary excretion had long been regarded as a means by which animals could rid themselves of excess selenium. However, later work demonstrated that arsenic increased the biliary excretion of selenium. Not only did arsenic stimulate the excretion of selenium in the bile, but selenium also stimulated the excretion of arsenic in the bile. This increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of selenium, although the chemical mechanism by which arsenic does this is not certain. The most satisfactory explanation is that these two elements react in the liver to form a detoxication conjugate which is then excreted into the bile. This is consistent with the fact that both arsenic and selenium each increase the biliary excretion of the other. Several other metabolic interactions between arsenic and selenium have been demonstrated in vitro, but their physiological significance is not clear.

Although arsenic decreased selenium toxicity under most conditions, there is a pronounced synergistic toxicity between arsenic and two methylated selenium metabolites, trimethylselenonium ion or dimethyl selenide. The ecological consequences of these synergisms are largely unexplored, although it is likely that selenium methylation occurs in the environment.

All attempts to promote or prevent selenium deficiency diseases in animals by feeding arsenic have been unsuccessful.

Over 30 years ago it was suggested that industrial hygienists use arsenic as a tonic to prevent or cure selenium poisoning in workers exposed to this hazard. Organic arsenical feed additives were tried as partial antidotes against selenium poisoning in livestock raised in seleniferous agricultural areas but were not found to be practical.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Bunyan J., Diplock A. T., Cawthorne M. A., Green J. Vitamin E and stress. 8. Nutritional effects of dietary stress with silver in vitamin E-deficient chicks and rats. Br J Nutr. 1968 May;22(2):165–182. doi: 10.1079/bjn19680023. [DOI] [PubMed] [Google Scholar]
  2. GANTHER H. E., BAUMANN C. A. Selenium metabolism. I. Effects of diet, arsenic and cadmium. J Nutr. 1962 Jun;77:210–216. doi: 10.1093/jn/77.2.210. [DOI] [PubMed] [Google Scholar]
  3. HENDRICK C., KLUG H. L., OLSON O. E. Effect of 3-nitro-4-hydroxyphenylarsonic acid and arsanilic acid on selenium poisoning in the rat. J Nutr. 1953 Sep;51(1):131–137. doi: 10.1093/jn/51.1.131. [DOI] [PubMed] [Google Scholar]
  4. Holmberg R. E., Jr, Ferm V. H. Interrelationships of selenium, cadmium, and arsenic in mammalian teratogenesis. Arch Environ Health. 1969 Jun;18(6):873–877. doi: 10.1080/00039896.1969.10665508. [DOI] [PubMed] [Google Scholar]
  5. KLUG H. L., MOXON A. L., PETERSEN D. F. The in vivo inhibition of succinic dehydrogenase by selenium and its release by arsenic. Arch Biochem. 1950 Sep;28(2):253–259. [PubMed] [Google Scholar]
  6. Levander O. A., Argrett L. C. Effects of arsenic, mercury, thallium, and lead on selenium metabolism in rats. Toxicol Appl Pharmacol. 1969 Mar;14(2):308–314. doi: 10.1016/0041-008x(69)90112-4. [DOI] [PubMed] [Google Scholar]
  7. Levander O. A., Baumann C. A. Selenium metabolism. V. Studies on the distribution of selenium in rats given arsenic. Toxicol Appl Pharmacol. 1966 Jul;9(1):98–105. doi: 10.1016/0041-008x(66)90034-2. [DOI] [PubMed] [Google Scholar]
  8. Levander O. A., Baumann C. A. Selenium metabolism. VI. Effect of arsenic on the excretion of selenium in the bile. Toxicol Appl Pharmacol. 1966 Jul;9(1):106–115. doi: 10.1016/0041-008x(66)90035-4. [DOI] [PubMed] [Google Scholar]
  9. Levander O. A., Morris V. C., Higgs D. J. Acceleration of thiol-induced swelling of rat liver mitochondria by selenium. Biochemistry. 1973 Nov 6;12(23):4586–4590. doi: 10.1021/bi00747a007. [DOI] [PubMed] [Google Scholar]
  10. Levander O. A., Morris V. C., Higgs D. J. Selenium as a catalyst for the reduction of cytochrome c by glutathione. Biochemistry. 1973 Nov 6;12(23):4591–4595. doi: 10.1021/bi00747a008. [DOI] [PubMed] [Google Scholar]
  11. McCONNELL K. P., PORTMAN O. W. Excretion of dimethyl selenide by the rat. J Biol Chem. 1952 Mar;195(1):277–282. [PubMed] [Google Scholar]
  12. McCONNELL K. P., PORTMAN O. W. Toxicity of dimethyl selenide in the rat and mouse. Proc Soc Exp Biol Med. 1952 Feb;79(2):230–231. doi: 10.3181/00379727-79-19333. [DOI] [PubMed] [Google Scholar]
  13. Moxon A. L. THE EFFECT OF ARSENIC ON THE TOXICITY OF SELENIFEROUS GRAINS. Science. 1938 Jul 22;88(2273):81–81. doi: 10.1126/science.88.2273.81. [DOI] [PubMed] [Google Scholar]
  14. Muth O. H., Whanger P. D., Weswig P. H., Oldfield J. E. Occurrence of myopathy in lambs of ewes fed added arsenic in a selenium-deficient ration. Am J Vet Res. 1971 Oct;32(10):1621–1623. [PubMed] [Google Scholar]
  15. Obermeyer B. D., Palmer I. S., Olson O. E., Halverson A. W. Toxicity of trimethylselenonium chloride in the rat with and without arsenite. Toxicol Appl Pharmacol. 1971 Oct;20(2):135–146. doi: 10.1016/0041-008x(71)90040-8. [DOI] [PubMed] [Google Scholar]
  16. PATTERSON E. L., MILSTREY R., STOKSTAD E. L. Effect of selenium in preventing exudative diathesis in chicks. Proc Soc Exp Biol Med. 1957 Aug-Sep;95(4):617–620. doi: 10.3181/00379727-95-23307. [DOI] [PubMed] [Google Scholar]
  17. Palmer I. S., Arnold R. L., Carlson C. W. Toxicity of various selenium derivatives to chick embryos. Poult Sci. 1973 Sep;52(5):1841–1846. doi: 10.3382/ps.0521841. [DOI] [PubMed] [Google Scholar]
  18. Scott M. L., Olson G., Krook L., Brown W. R. Selenium-responsive myopathies of myocardium of smooth muscle in the young poult. J Nutr. 1967 Apr;91(4):573–583. doi: 10.1093/jn/91.4.573. [DOI] [PubMed] [Google Scholar]
  19. Walker G. W., Bradley A. M. Interacting effects of sodium monohydrogenarsenate and selenocystine on crossing over in Drosophila melanogaster. Can J Genet Cytol. 1969 Sep;11(3):677–688. doi: 10.1139/g69-081. [DOI] [PubMed] [Google Scholar]

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