This study was carried out to elucidate the toxic mechanism of cadmium in peripheral nerve. An animal model of cadmium neuropathy was induced by feeding diet containing cadmium to Sprague- Dawley rat (or two weeks. Four weeks aged Sprague- Dawley rats were divided into four groups : normal control group, 10ppm- cadmium treated group, 100ppm- cadmium treated group, 1000ppm- cadmium treated group, reference drug- treated group. All rats were sacrificed at the end of two weeks for assessing the development of cadmium neuropathy, These results obtained were summarized as follows : 1. Cadmium reduced peripheral flow of both acetylcholinesterase and cholinesterase in rat sciatic nerve. 2. The toxic mechanism of cadmium might be the result of an reduction of myo-inositol concentration in peripheral nervous system 3. Reduction in myo-inositol content of peripheral nerve resulted from the inhibition of sodium- Potassium ATPase activity, which is responsible for myo-inositol transport, by cadmium 4. Oral administration of myo-inositol improved the flow of both acetylcholinesterase and cholinesterasenerve in cadmium intoxicated rat. These results suggest that mild cadmium neuropathy might be diagnosed by checking nervous myo-inositol content and oral administraion of myo-inositol might prevent the development of severe cadmium neuropathy with special reference to detective axonal transport.