ABSTRACT
I. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 II. Cyanide Exposure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302
III. Symptoms Produced by Cyanide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303 IV. Chemical Reactivity of Cyanide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305 V. Metabolism of Cyanide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306
VI. Effects of Cyanide on Neural Tissue. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308 A. Elevated Cell Calcium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 308 B. Effects of Cyanide on Metabolism of Neurons . . . . . . . . . . . . . . . . . . . 308 C. Oxidative Stress in Neuronal Cells and Cyanide. . . . . . . . . . . . . . . . . . 308 D. Hyperpolarization by Cyanide. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309 E. Neuronal Activation by Cyanide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310
VII. Effects of Cyanide on the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310 VIII. ADP-Ribosylation by Cyanide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312
IX. Production of Cyanide in Neural Tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 X. Cyanide Antidotes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313
XI. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313 Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314
Since the previous report in 1992, important new findings have provided fresh insight into CN mechanisms of action in both neural and cardiac tissue, the primary targets of CN intoxication.1 Most studies use CN to produce chemical hypoxia or to mimic conditions caused by stroke and myocardial infarction. Generally, actions of CN resemble those of ischemia and hypoxia, so information gained from CN studies is as important for the analysis of the chemical itself as for study of common pathological conditions.2 –5
Not only is CN acutely toxic in high (mg) doses, serious neurological problems are associated with chronic exposure at lower levels.6 This review also includes recent observations on this timely issue.
