Biomedical subjects

W R MARTIN

Publications and source records attributed to W R MARTIN.

At least 19 recordsLinked to original sources

PubMed1965

6-DIAZO-5-OXO-L-NORLEUCINE INHIBITION OF ESCHERICHIA COLI.

Coggin, J. H., Jr. (The University of Chicago, Chicago, Ill.), and W. R. Martin. 6-Diazo-5-oxo-l-norleucine inhibition of Escherichia coli. J. Bacteriol. 89:1348-1353. 1965.-The glutamine analogue 6-diazo-5-oxo-l-norleucine (DON) induced filaments and spheroplasts in Escherichia coli during the transition of sensitive populations to a state of resistance. Resistance developed at a frequency suggesting mutant selection. The morphology of cells resistant to 100 mug of DON per ml was indistinguishable from that of sensitive cells. DON-resistant cells exhibited an extended growth lag when cultured in the absence of the drug. This extended lag could be reduced to the lag time of parent sensitive cells by a combination of d-glucosamine and inosine or by DON. Viable counts during the lag period of resistant cells indicate that this lag results from a decrease in the number of cells during the first 2 hr of incubation. A combination of d-glucosamine and inosine was required for complete prevention of the DON inhibition of sensitive cells. The results indicate that DON not only inhibits de novo purine biosynthesis but that it also prevents hexosamine synthesis and, ultimately, cell-wall synthesis in E. coli.

Antimetabolites↗

PubMed1964

RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION. I. FACTORS WHICH INTERFERE WITH THE INITIATION OF INFECTION BY ORAL INOCULATION.

Multiplication of Salmonella enteritidis was inhibited in vitro by buffered suspensions of fecal material freshly removed from the large intestine of normal mice. Most effective was material obtained from cecum and transverse colon. Inhibitory activity was not impaired by sterilization by heat or filtration. From such materials were isolated acetic and butyric acids in concentrations which inhibited Salmonella in vitro. The degree of inhibitory activity of suspensions of colon content and of mixtures of the two fatty acids was conditioned by pH and favored by anaerobiosis. Effective inhibition occurred at or slightly below the pH of colon content of most normal mice as determined in situ by direct measurement. Acetic and butyric acids were isolated from anaerobic cultures of several strains of Bacteroides previously demonstrated to be one of the most numerous inhabitants of the large intestine of the normal mouse.

Acetates↗

PubMed1964

RESISTANCE OF THE MOUSE'S INTESTINAL TRACT TO EXPERIMENTAL SALMONELLA INFECTION. II. FACTORS RESPONSIBLE FOR ITS LOSS FOLLOWING STREPTOMYCIN TREATMENT.

Determinations of pH, Eh, and concentrations of acetic, butyric and lactic acids were made on the content of cecum and transverse colon of groups of mice killed 1, 3, and 5 days after oral administration of 50 mg streptomycin. Control observations on untreated mice are reported in the preceding communication. Heat-killed supenatants of suspensions of bowel content were tested in vitro for their ability to inhibit multiplication of our standard streptomycin-resistant strain of Salmonella enteritidis during aerobic and anaerobic incubation. Also tested in like fashion were series of cultures in broth buffered at various pH levels and containing acetic, butyric, and lactic acids in varying concentrations. In colon content of mice on the 1st day after streptomycin treatment, the pH had risen and the concentrations of the fatty acids fallen, a combination of effects which adequately accounts for its inability to inhibit multiplication of Salmonella in vitro and in vivo. By the 3rd day after streptomycin treatment, pH and fatty acid concentrations had returned to normal levels. The susceptibility of mice to oral challenge on the 3rd day was explained by the finding that lactic acid had accumulated in colon content to levels which, in broth, effectively counteracted the activity of inhibitory concentrations of the fatty acids. Other cocarboxylic acids also antagonized the inhibitory activity of the fatty acids; glucose did not.

Acetates↗

PubMed1964