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Pharmacologic Role of Cysteine in Ameliorating or Exacerbating Mineral Toxicities¹

Department of Animal Sciences and Division of Nutritional Sciences, University of Illinois, Urbana, IL 61801

Cysteine, via chelation reactions, ameliorates biochemical lesions caused by excessive ingestion of several trace elements. Because oral cysteine per se is considerably more protective than the in vivo metabolic cysteine precursors, methionine or cystine, chelation of cysteine with trace elements likely occurs primarily in the gut, thereby decreasing absorption of both cysteine and the trace element in question. Hence, using copper as an example, orally administered cysteine markedly improves growth and reduces liver copper deposition in chicks or rats fed a high level of inorganic copper. Likewise, excessive copper ingestion impairs sulfur amino acid (SAA) utilization and increases the dietary requirement for SAA. Cobalt and selenium toxicities are also ameliorated by oral cysteine ingestion, with the responses being even more striking than those occurring with copper toxicity. While inorganic arsenic poisonings are generally ameliorated by administering cysteine or a cysteine derivative (e.g., dimercaptopropanol), organic pentavalent arsenic toxicity is exacerbated by cysteine administration. Cysteine in this instance acts as a reducing agent, facilitating conversion of organic pentavalent arsenicals such as roxarsone and arsanilic acid to the more toxic trivalent state.

KEY WORDS: • cysteine • methionine • metal • chelation • copper • cobalt • selenium • arsenic • roxarsone • chick • rat

¹ Dr. Baker received the 1986 Borden Award in Nutrition and was invited to write this review of the work upon which his award was based.

Manuscript received 20 November 1986. Revision accepted 12 February 1987.

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