Dietary deficiency of cystine and methionine in rats alters thiol homeostasis required for cyanide detoxification

John Tor-Agbidye, Valerie S. Palmer, Mohammad I. Sabri, A. Morrie Craig, Linda L. Blythe, Peter S. Spencer

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Nutritional status is an important factor in modulating the metabolic fate of xenobiotics. Sulfur amino acid (SAA) deficiency has been proposed as a risk factor for human neurological diseases among protein-poor populations subsisting on the cyanophoric plant cassava. Female Sprague-Dawley rats were used to develop and define a model of SAA deficiency for use in future studies examining cassava-related neurotoxicity. Rats were kept in metabolic cages for 7-21 d and fed a balanced diet (BD) of known composition or a comparable diet selectively deficient in methionine and cystine (SAA-free diet). Animals fed the SAA-free diet failed to thrive, lost body weight, excreted porphyrinic materials, and showed a steep and persistent reduction of urinary inorganic sulfate. In contrast, animals on the BD gained body weight and maintained baseline output of urinary inorganic sulfate. Urinary thiocyanate excretion did not differ between groups, but plasma thiocyanate concentrations reached double that in SAA-deficient rats. Increased plasma thiocyanate suggests mobilization of sulfur amino acids from endogenous sources. Liver glutathione and blood cyanide concentrations were similar in animals on the BD and the SAA-deficient diet. In summary, a diet free of methionine and cystine results in increased retention of inorganic sulfur as thiocyanate and a near absence of inorganic sulfur excretion in urine.

Original languageEnglish (US)
Pages (from-to)583-595
Number of pages13
JournalJournal of Toxicology and Environmental Health - Part A
Issue number8
StatePublished - 1998

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis


Dive into the research topics of 'Dietary deficiency of cystine and methionine in rats alters thiol homeostasis required for cyanide detoxification'. Together they form a unique fingerprint.

Cite this