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Biomedical subjects

M FORBES

Publications and source records attributed to M FORBES.

At least 19 recordsLinked to original sources
PubMed1965

EFFECT OF ETHAMBUTOL ON NUCLEIC ACID METABOLISM IN MYCOBACTERIUM SMEGMATIS AND ITS REVERSAL BY POLYAMINES AND DIVALENT CATIONS.

Forbes, M. (Lederle Laboratories Division, Pearl River, N.Y.), N. A. Kuck, and E. A. Peets. Effect of ethambutol on nucleic acid metabolism in Mycobacterium smegmatis and its reversal by polyamines and divalent cations. J. Bacteriol. 89:1299-1305. 1965.-Mycobacterium smegmatis, harvested from cultures inhibited by ethambutol and then suspended in drug-free medium, exhibited a prolonged lag before growth resumed. Polyamines and magnesium ions shortened this lag. Polyamines and magnesium added to the culture increased the minimal inhibitory concentration of the drug and reversed the inhibitory effect of the drug, even when added after the drug had already inhibited growth. When ethambutol was added to a culture in its exponential phase of growth, synthesis of protein and deoxyribonucleic acid (DNA), as measured by incorporation of S(35) and P(32), continued for 3 hr at a rate slightly less than in the control cells and then essentially ceased. Synthesis of ribonucleic acid (RNA) was depressed, but it proceeded even after protein synthesis had ceased. Even though the synthesis of RNA continued, the net RNA decreased, and inhibited cells became deficient in RNA. Polyamines and divalent cations, which reverse the inhibitory effect of the drug, have been reported to be involved in nucleic acid turnover. These considerations suggested that ethambutol may exert its inhibitory effect by interfering with a function of cellular polyamines and divalent cations in RNA metabolism.

Amines↗
PubMed1962

Mode of action of ethambutol.

Forbes, M. (Lederle Laboratories Division, Pearl River, N.Y.), N. A. Kuck, and E. A. Peets. Mode of action of ethambutol. J. Bacteriol. 84:1099-1103. 1962.-Ethambutol [2,2'-(ethylenediimino) di-1-butanol] arrested multiplication of Mycobacterium smegmatis cells and eventually effected their death. The inhibitory effect of the drug on multiplication did not become apparent until several hours after its addition to the culture. The drug had no effect on the survival of nonproliferating cells. It had little or no effect on the metabolism of nonproliferating cells, but cells from cultures whose growth had been inhibited by ethambutol showed evidence of impaired metabolism. C(14)-labeled ethambutol was taken up rapidly by both proliferating and nonproliferating cells. The observations are consistent with the hypothesis that ethambutol exerts its antibacterial effect by interfering with the synthesis of a metabolite(s) needed for multiplication. Depletion of the metabolite(s) results in arrest of multiplication, impairment of metabolism, and loss of viability. Resistance to ethambutol cannot be explained by the failure of the cells to take up the drug, since the drug was equally bound by resistant and sensitive cells.

Antitubercular Agents↗
PubMed1961

Experimental Shigella infections. V. Studies in germ-free guinea pigs.

Formal, Samuel B., (Walter Reed Army Institute of Research, Washington, D. C.), Gustave Dammin, Helmuth Sprinz, Donald Kundel, Herman Schneider, Richard E. Horowitz, and Martin Forbes. Experimental shigella infections. V. Studies in germ-free guinea pigs. J. Bacteriol. 82:284-287. 1961.-Germ-free guinea pigs succumb after oral infection with Shigella flexneri serotype 2a; they survive a similar challenge with either a strain of Escherichia coli or a culture of lactobacillus. Animals monocontaminated with E. coli survive, whereas those monocontaminated with lactobacilli succumb to subsequent challenge with dysentery bacilli. Prior subcutaneous inoculation of heat-killed S. flexneri 2a does not render germ-free guinea pigs resistant to the fatal infection with viable dysentery bacilli.

Animals↗