Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical-generating divalent cation manganese and deficiencies of antioxidant co factors Cu, Se, Fe, Zn. Does a foreign cation substitution at prion protein's Cu domain initiate TSE?

Medical Hypotheses

Volumn 54, Issue 2, 2000, Pages 278-306

  Purdey, M ^a  

^a NONE

Author keywords

[No Author keywords available]

Indexed keywords

ANTIOXIDANT; CATION; CONCANAVALIN A; COPPER; GLYCOPROTEIN; INSECTICIDE; IRON; MANGANESE; MANGANESE SUPEROXIDE DISMUTASE; MEMBRANE PROTEIN; METALLOPROTEIN; OXIDIZING AGENT; PHOSPHORUS; PRION PROTEIN; SELENIUM; SODIUM; ZINC;

ABSORPTION; ARTICLE; ASTROCYTE; AUTOOXIDATION; BOVIDS; BOVINE SPONGIFORM ENCEPHALOPATHY; CAPPING PHENOMENON; CENTRAL NERVOUS SYSTEM; CONCENTRATION (PARAMETERS); CREUTZFELDT JAKOB DISEASE; ECOSYSTEM; FOOD CHAIN; GENOTYPE; HUMAN; ICELAND; MINERAL BALANCE; MITOCHONDRION; NERVE DEGENERATION; NEUROTOXICITY; NONHUMAN; OXIDATION; PRENATAL EXPOSURE; PRION DISEASE; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN CONFORMATION; PROTEIN DOMAIN; PROTEIN MODIFICATION; SCRAPIE; SLOVAKIA; UNITED STATES;

BOVIDAE; BOVINAE; EQUUS CABALLUS;

EID: 0034018313     PISSN: 03069877     EISSN: None     Source Type: Journal    
DOI: 10.1054/mehy.1999.0836     Document Type: Article

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