Cytoplasmic membrane: bacterial

Considerable work has been done to try to explain why quats are antimicrobial. The following sequence of steps is beheved to occur in the attack by the quat on the microbial cell (/) adsorption of the compound on the bacterial cell surface (2) diffusion through the cell wall (J) binding to the cytoplasmic membrane (4) dismption of the cytoplasmic membrane (5) release of cations and other cytoplasmic cell constituents (6) precipitation of cell contents and death of the cell. 

Furthermore, if the antibiotic passes membranes through a specific port of entry, its mutational loss leads to resistance. The lack of the outer membrane protein OprD in P. aeruginosa causes resistance to the (3-lactam antibiotic imipenem. Fosfomycin passes the cytoplasmic membrane via an L-a-glycerol phosphate permease. This transport system is not essential for bacterial growth and therefore mutants with a reduced expression are frequently selected under therapy. 

Proteins identified by their ability to bind labelled (3-lactam antibiotics in vivo and in vitro. The intrinsic activities of PBPs include transglycosylase/transpepti-dase, carboxypeptidase and endopeptidase activities required for the formation of the bacterial murein sacculus forming the bacterial cell wall. The enzymes are located in the cytoplasmic membrane. 

FIG. 14 Schematic illustration of an archaeal cell envelope structure (a) composed of the cytoplasmic membrane with associated and integral membrane proteins and an S-layer lattice, integrated into the cytoplasmic membrane, (b) Using this supramolecular construction principle, biomimetic membranes can be generated. The cytoplasmic membrane is replaced by a phospholipid or tetraether hpid monolayer, and bacterial S-layer proteins are crystallized to form a coherent lattice on the lipid film. Subsequently, integral model membrane proteins can be reconstituted in the composite S-layer-supported lipid membrane. (Modified from Ref. 124.)... 

Three fundamental divisions of the bacterial cell occur in all species cell wall, cell or cytoplasmic membrane, and cytoplasm. 

Cytoplasmic membrane Polymyxins Polyenes Imidazoles and triazoles Naftidine Disrupt bacterial membranes Disrupt fungal membranes Inhibit ergosterol synthesis Inhibits ergosterol synthesis Bind to LPS and phospholipids Bind preferentially to ergosterol Pathway not in mammalian cells Pathway not in mammalian cells... 

Treatment of bacterial cells with appropriate concentrations of such substances as eetrimide, chlorhexidine, phenol and hexylresorcinol, causes a leakage of a group of eharacteristic chemical species. The potassium ion, being a small entity, is the fust substance to appear when the cytoplasmic membrane is damaged. Amino acids, purines, pyrimidines and pentoses are examples of other substances which will leak horn treated cells. 

Ivanov, A.I., Fomchenkov, V.M., Khasanova, L.A., and Gavriushkin, A.V., Toxic effect of hydroxylated ions of heavy metals on the cytoplasmic membrane of bacterial cells, Mikrobiologiia, 66 (5), 588-594,1997. 

Saurin, W., Koster, W. and Dassa, E. (1994). Bacterial binding protein-dependent permeases characterization of distinctive signatures for functionally related integral cytoplasmic membrane proteins, Mol. Microbiol., 12, 993-1004. 

ATP synthesis is the final step in the conservation of energy via chemios-mosis. This step is catalyzed by FiFo ATP synthase, a multisubunit enzyme complex found exclusively in cytoplasmic membranes of bacteria (Senior 1988). It uses the chemiosmotic energy (ApH) generated from membrane ET to synthesize ATP from ADP and Pi. The most investigated bacterial... 

Haukland, H. H., Ulvatne, H., Sandvik, K., and Vorland, L. H. (2001). The antimicrobial peptides lactoferricin B and magainin 2 cross over the bacterial cytoplasmic membrane and reside in the cytoplasm. FEES Lett. 508, 389-393. 

The bacterial cell wall is a rigid outer layer that completely surrounds the cytoplasmic membrane. Penicillin and other betalactam antibiotics inhibit bacterial growth by interfering with a specific step in bacterial cell wall synthesis. Penicillins are classified as in table 9.3.1. 

All aminoglycosides act by inhibiting protein synthesis of bacteria by directly combining with ribosomes. They penetrate the outer cytoplasmic membrane and inhibit protein synthesis. Streptomycin combines with the bacterial 30S ribosomes and inteferes with the mRNA-ribosome combination. Other aminoglycosides bind to additional sites on SOS subunit as well as to 30S-50S interface. 

It is bactericidal drug and exerts its action by combining with bacterial ribosome and induces misreading of mRNA codons. Also in sensitive bacteria, disruption of cytoplasmic membrane occurs resulting in leakage of amino acids, ions, leading to bacterial death. 

In other bacteria, such as Acinetobacter, alkane oxidation genes are chromosomal (Singer Finnerty, 1984b). Moreover, some of the genes that participate in alkane oxidation probably comprise indispensable constituents of the bacterial cell. For example, in P. oleovorans, one of the gene products that catalyzes the initial oxidation of aliphatic substrates, the alkane hydroxylase, is an integral cytoplasmic membrane protein, and constitutes after induction 1.5-2% of the total cell protein (Nieboer et al. 1993). 

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