VPT 421: Veterinary Toxicology (2+0)

MECHANISM OF TOXICITY

• Excess cyanide in blood and tissues bind to ferric iron of cytochrome oxidase and prevent the transfer of electrons.
  • Cyanide ion reacts with Fe ⁺³ (ferric) ion of cytochrome oxidase to form a stable complex.
  • Conversion of Fe ⁺³ to Fe ⁺² is thereby prevented so that electron transport and cellular respiration are stopped. The blood is oxygenated, but cannot be utilized by the cells.
  • The lack of O ₂ utilization in chemoreceptors and/or neurons of the brain triggers increased respiratory efforts and the blood becomes hyperoxygenated ("bright red").
  • End result is a functional tissue anoxia.

• Cells die from lack of usable oxygen. This results in tissue anoxia with serious effects in the brain.
• In the brain, cyanide decreases oxidative metabolism,increases glycolysis, and inhibits brain glutamic acid decarboxylase, thereby decreasing gamma aminobutyric acid (GABA).
• The corpus callosum, hippocampus, corpora striata, and substantia nigra are commonly damaged in cyanide poisoning.
• Death in acute cases occurs within a few seconds.