[Cyanide with vitamin B12 deficiency as the cause of experimental tobacco amblyopia]

The visual toxicity of tobacco smoke was studied and demyelination change of retrobulbar portion of the rat's optic nerve with an elongation of a peak latency time of visual evoked potentials (VEP) was demonstrated. Cyanide detoxication incapacity and deficiency of vitamin B12 (B12) have been considered as possible causes of tobacco amblyopia. In order to elucidate an influence of cyanide poisoning and B12 deficiency on the visual system, 12 male Wistar rats were subjected to 5 hour's daily inhalation of cyanide gas for 52 weeks, the concentration of which was adjusted to that of tobacco smoke. Six rats of these 12 were fed with a lacking B12 diet. Another 12 male Wistar rats were controls which did not undergo inhalation of cyanide gas, and half of them were fed a diet without B12. In 2 out of 6 rats with cyanide and inhalation and B12 deficiency, demyelination change could be recognized in the central portion of the retrobulbar optic nerve. The histological change was segmental and significant elongation of the peak latency time of VEP was not recognized. Cyanide gas inhalation at a low concentration was proved to be harmful to the optic nerve under the condition of B12 deficiency, but other toxic elements such as nicotine and carbon monoxide may be important factors to cause the more severe changes of the optic nerve with an abnormal VEP response recognized in the experimental tobacco amblyopia.