ACETIC ACID OXIDATION BY ESCHERICHIA COLI: EVIDENCE FOR THE OCCURRENCE OF A TRICARBOXYLIC ACID CYCLE
ACETIC ACID OXIDATION BY ESCHERICHIA COLI: EVIDENCE FOR THE OCCURRENCE OF A TRICARBOXYLIC ACID CYCLE
复制标题
大肠杆菌的乙酸氧化:三羧酸循环发生的证据
作者:
H. Swim;L. Krampitz
The tricarboxylic acid cycle has received general acceptance as a mechanism to explain the oxidation of acetic acid by animal tissues. The data obtained in studies with bacteria do not satisfy many of the criteria on which the cycle was based in animal tissues (Krebs, 1948-1949). In the preceding report, Saz and Krampitz (1954) critically evaluated this problem as applied to bacteria. Techniques were described which permit the isolatioga of intermediates of acetate oxidation in the absence of added carriers. These intermediates were in approximately complete isotopic equilibrium with each other, with the recovered acetate, and with the respiratory carbon dioxide. These data were in contrast with the results obtained with carrier experiments employing Micrococcus lydeikticu (Saz and Krampitz, 1950; Ajl and Kamen, 1950) and Escherichia coli (Swim and Krampitz, 1950; Ajl and Kamen, 1950). In the latter case, isotope from acetate-2-C4 was not incorporated into a-ketoglutarate to a significant extent. The carrier succinate, on the other hand, was highly radioactive, and the carboxyl carbons were in almost complete isotopic equilibrium with the respiratory carbon dioxide. These data could be interpreted as evidence that the tricarboxylic acid cycle is of no quantitative importance as a mechani for the oxidation of acetate by E. coli and that the major mechanism involves acetate condensation to succinate (Thunberg condensation) and the other reactions of the dicarboxylic acid cycle. It has been shown by Saz and Krampitz (1954) that nonequilibration between metabolic a-ketoglutarate and that added as a carrier can account for the observed results, and, therefore, the evidence for the dicarboxylic acid cycle was unsatisfactory. The results of experiments