Abstract
Biological significance of sulfur-containing amino acids in the body has gradually become recognized in recent years but majority of studies made on them has been fundamental and examinations as to their relationship to clinical pathology have been left for future work.
As a part of studies on the mechanism of ethionine damage, metabolism of sulfurcontaining amino acids chiefly in the liver and the pancreas was examined, using (S35) methionine as a tracer.
Summarized results thereby obtained were as follows:
1)(S35) Methionine was administered intraperitoneally to normal mice and the amout of the amino acid consumed by each organ was examined by measuring radioactivity.There was a fairly great diflerence between the organs. The amount of the labeled amino acid was generally greater in the organs with strong metabolic activity, such as the liver, pancreas, kidneys, and intestines, and extremely small in the muscles and the skin.
2) Methionine is metabolized in the body down to inorganic sulfate and excreted but ethionine is not metabolized and the majority is excreted into the urine. Chromatography of organ proteins has shown that incorporation of ethionine into organ proteins is detected even 3 days after administration, when detection in the non-protein portion becomes difficult. The incorporation is especially marked in the liver and pancreas and the fact agrees with the high incidence of damage in these two organs.
3) Experiments both in vivo and in vitro have shown that incorporation of (S35) methionine into the liver and pancreas proteins is suppressed by ethionine.
4) Perfusion of rat liver with a solution containing (S35) methionine and measurement of radioactivity of the proteins in the perfusion fluid showed that incorporation of (S35) methionine at the time of plasma protein synthesis in the liver is also interfered by ethionine.
5) The course of metabolism of (S
35) methionine in the hepatic and pancreatic tissues was examined by radiochromatography of the tissue hydrolyzate. No detailed results were revealed on individual intermediate metabolites but metabolism of (S35) methionine seemed to be interfered by ethionine.
6) The same experiments were carried out on animals damaged by carbon tetrachloride and chloroform, and it was learned that there was no suppression of (S53) methionine incorporation into the liver proteins. Metabolic decomposition of (S35) methionine in the tissue also did not show any definite tendency of suppression as in the case of ethionine damage.
