Effects of Antibiotics on Metabolism of Peptidoglycan, Protein, and Lipids in Bifidobacterium bifidum subsp. pennsylvanicus
Author(s) -
G. C. Molenkamp,
J.H. Veerkamp
Publication year - 1976
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.10.5.786
Subject(s) - peptidoglycan , biochemistry , cell envelope , lipid ii , bacitracin , biology , cell wall , bifidobacterium bifidum , antibiotics , bifidobacterium , lactobacillus , escherichia coli , fermentation , gene
The formation of cell envelope components of Bifidobacterium bifidum subsp. pennsylvanicus was studied by measuring the incorporation of [(3)H]glycine, (14)C-labeled fatty acids, and N-benzoyl-[(14)C]glucosamine into the membrane protein, membrane lipids, and cell wall peptidoglycan, respectively. Inhibition of peptidoglycan synthesis by antibiotics (penicillin G, vancomycin, d-cycloserine, and bacitracin) and by the omission of glucosamine-containing growth factors caused a marked decrease in glycine incorporation into cellular as well as membrane protein, which was accompanied by a considerable enhancement of fatty acid incorporation. The uncoupling of protein and lipid synthesis led to the release of marked amounts of lipids from the cell under these conditions. Arrestment of protein synthesis by antibiotics (chloramphenicol, tetracycline, and actinomycin D) decreased peptidoglycan and lipid synthesis only partially, but did not lead to lipid release. Mg(2+) deficiency of the medium caused about 60% inhibition of growth and lipid synthesis, but protein synthesis and especially peptidoglycan synthesis were much less inhibited. Staphylococcin 1580 arrested the growth and also the synthesis of protein and peptidoglycan. However, the synthesis and turnover of lipids were considerably increased and a release of large amounts of lipids was observed. Peptidoglycan and cellular protein did not show any turnover either during normal growth or after the inhibition of cell wall and protein synthesis.
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