Recently, chinoform has come to attract the attention as one of the etiologic factors of the disease, subacute myelo-optico neuropathy commonly known as SMON in Japan. For the purpose to study the metabolism of chinoform in vivo, a series of experiments were conducted with labeled chinoform ((131)I-chinoform) with rats of Wistar strain. As a step to increase the toxicity of chinoform, carbon tetrachloride was administered to the rats to induce liver disturbances as to increase the chinoform retention in vivo, and as another step rabbit-antirat kidney serum was injected to the animals so as to elicit allergic nephritis, and then (131)I-chinoform was intravenously injected each of these two groups of animals. The next procedure was to analyze the in vivo distribution of (131)I-chinoform. The results of the study are briefly summarized as follows. In the case administered with carbon tetrachloride practically all the central nervous system and the sciatic nerve revealed a higher radioactivity of free chinoform, and also the percentage of free chinoform to the total chinoform was greater as revealed by the radioactivity of the chloroform-soluble fraction. By microautoradiography, labeled chinoform was detected in Purkinje cells and glial cells in the molecular layer of the cerebellum, glial cells of the thalamus as well as the brain stem, and in the posterior root ganglia, anterior horn cells and meninges of the spinal cord. In the liver it was observed in Kupffer stellate cells and cholangioli and slightly in hepatic cells. As for the kidney, the labeled chinoform was markedly incorporated in the proximal convoluted tubuli and slightly in the glomeruli. Next, in the rats with experimental nephritis, the decreasing rate of radioactivity in the blood was relatively low as compared with that of the control group. In the kidneys the radioactivity was high in the total fraction, chloroform-soluble fraction and chloroform-insoluble fraction as compared with respective values in the controls, showing 30 to 50-fold values.