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1 From the Departments of Internal Medicine and Pathological Chemistry of the Southwestern Medical College and Parkland Hospital, Dallas, Texas, and the Department of Biochemistry, Cornell University Medical College, New York, N. Y.
The possible relationship between the mechanisms of the liver and kidney injury produced by certain toxic substances, and the mechanisms of similar injury produced by feeding diets deficient in choline and methionine, was discussed.
The already methylated product of pyridine, methyl pyridinium chloride, when fed in the diet to rats, did not produce liver and kidney injury such as was observed with equivalent concentrations of pyridine.
When methyl pyridinium chloride was fed to rats, it was easily recovered from the urine, but when pyridine was administered, the methylated product was not found in the urine. This observation, together with the previously reported ineffectiveness of choline, but effectiveness of cystine, in affording protection against pyridine injury, was considered substantial evidence against a drainage of methyl groups as the mechanism of the liver and kidney damage produced by pyridine in the rat, and also against the content of labile methyl groups as the explanation of the protective effect of methionine under these circumstances.
Submitted on August 12, 1947