<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tor-Agbidye, J</style></author><author><style face="normal" font="default" size="100%">Palmer, V S</style></author><author><style face="normal" font="default" size="100%">Lasarev, M R</style></author><author><style face="normal" font="default" size="100%">Craig, A M</style></author><author><style face="normal" font="default" size="100%">Blythe, L L</style></author><author><style face="normal" font="default" size="100%">Sabri, M I</style></author><author><style face="normal" font="default" size="100%">Spencer, P S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Bioactivation of cyanide to cyanate in sulfur amino acid deficiency: relevance to neurological disease in humans subsisting on cassava.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicological sciences : an official journal of the Society of Toxicology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicol. Sci.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyanates</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyanides</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystine</style></keyword><keyword><style  face="normal" font="default" size="100%">Diuresis</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Manihot</style></keyword><keyword><style  face="normal" font="default" size="100%">Methionine</style></keyword><keyword><style  face="normal" font="default" size="100%">Potassium Cyanide</style></keyword><keyword><style  face="normal" font="default" size="100%">Random Allocation</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Sprague-Dawley</style></keyword><keyword><style  face="normal" font="default" size="100%">Sulfates</style></keyword><keyword><style  face="normal" font="default" size="100%">Thiocyanates</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1999</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1999 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">50</style></volume><pages><style face="normal" font="default" size="100%">228-35</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Neurological disorders have been reported from parts of Africa with protein-deficient populations and attributed to cyanide (CN-) exposure from prolonged dietary use of cassava, a cyanophoric plant. Cyanide is normally metabolized to thiocyanate (SCN-) by the sulfur-dependent enzyme rhodanese. However, in protein-deficient subjects where sulfur amino acids (SAA) are low, CN may conceivably be converted to cyanate (OCN-), which is known to cause neurodegenerative disease in humans and animals. This study investigates the fate of potassium cyanide administered orally to rats maintained for up to 4 weeks on either a balanced diet (BD) or a diet lacking the SAAs, L-cystine and L-methionine. In both groups, there was a time-dependent increase in plasma cyanate, with exponential OCN- increases in SAA-deficient rats. A strongly positive linear relationship between blood CN- and plasma OCN- concentrations was observed in these animals. These data are consistent with the hypothesis that cyanate is an important mediator of chronic cyanide neurotoxicity during protein-calorie deficiency. The potential role of thiocyanate in cassava-associated konzo is discussed in relationship to the etiology of the comparable pattern of motor-system disease (spastic paraparesis) seen in lathyrism.</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/10478859?dopt=Abstract</style></custom1></record></records></xml>