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Article type: Research Article
Authors: Stearns, Diane M.;
Affiliations: Northern Arizona University, Department of Chemistry, P.O. Box 5698, Flagstaff, AZ 86011‐5698, USA
Note: [] Address for correspondence: Northern Arizona University, Department of Chemistry, P.O. Box 5698, Flagstaff, AZ 86011‐5698, USA. Tel.: +1 520 523 4460; Fax: +1 520 523 8111; E‐mail: [email protected].
Abstract: If chromium is an essential metal it must have a specific role in an enzyme or cofactor, and a deficiency should produce a disease or impairment of function. To date, no chromium‐containing glucose tolerance factor has been characterized, the purpose of the low‐molecular‐weight chromium‐binding protein is questionable, and no direct interaction between chromium and insulin has been found. Furthermore, chromium^{3+} is treated like the toxic metals arsenic, cadmium, lead and mercury in animals. Chromium^{3+} may be involved in chromium^{6+}‐induced cancers because chromium^{6+} is converted to chromium^{3+} in vivo, and chromium^{3+} is genotoxic and mutagenic. Although there is no direct evidence of chromium deficiencies in humans, dietary supplements exist to provide supraphysiological doses of absorbable chromium^{3+}. Chromium^{3+} may act clinically by interfering with iron absorption, decreasing the high iron stores that are linked to diabetes and heart disease. If so, this would make chromium^{3+} a pharmacological agent, not an essential metal.
Journal: Biofactors, vol. 11, no. 3, pp. 149-162, 2000
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