Drug resistance permeability changes

Chloramphenicol (Chloromycetin) is a nitrobenzene derivative that affects protein synthesis by binding to the 50S ribosomal subunit and preventing peptide bond formation. It prevents the attachment of the amino acid end of aminoacyl-tRNA to the A site, hence the association of peptidyltransferase with the amino acid substrate. Resistance due to changes in the ribosomebinding site results in a decreased affinity for the drug, decreased permeability, and plasmids that code for enzymes that degrade the antibiotic. 

Esterase formation is a mechanism of macrolide resistance seen in coliforms. Resistance to tetracyclines occurs either from increased activity of efflux mechanisms or changes in cell membrane permeability, leading to decreases in intracellular levels of such drugs. Resistance to chloramphenicol involves plasmid-mediated formation of drug-inactivating acetyltrans-ferases. The answer is (A). 

Actlnomvcin D - Kinetic studies with actinomycin D (act-D) in transplanted leukemic mice showed that a single dose provided cytotoxic concentrations for up to 24 hours,The characteristics of act-D resistance in L5178Y cells show that alterations in membrane composition and conformation in the drug-resistant subline accounts for the observed changes in the permeability of this drug.91 Act-D enhances the toxicity of morphine by increasing brain permeability. ... 

Phorbol esters are described to stimulate apical transcytosis probably via protein kinase C. These effects can be achieved by incubating cells with the tumor promoter PM A [1 pM (to 2pM)] for 30 minutes (to 60 minutes) (107,108). The total drug exposure time to about one hour because PMA shows an influence on tight junction permeability and thereby changes the transepithelial resistance. 

Two mechanisms of resistance have been discovered with respect to fluoroquinolones a change in subunits A of DNA-gyrase, and reduced permeability of the outer membrane of the bacteria. Resistance is mediated by chromosomes, and not plasmids in the bacteria. The development of resistance while using the drugs is very rarely observed. 

Resistance occurs by two mechanisms. Changes in bacterial permeability can hinder penetration of the drug or changes in the bacterial RNA polymerase can diminish drug binding to the enzyme. It is almost completely absorbed after oral administration with peak plasma concentrations reached after 2-A h. It... 

Resistance is related largely to changes in cell permeability and a resultant decreased accumulation of drug due to increased efflux from the cell by an energy-dependent mechanism. Other mechanisms, such as production of a protein that alters the interaction of tetracycline with the ribosome and enzymatic inactivation of the drug, have been reported. 

Resistance Occurring rarely, vancomycin resistance is due to plasmid-mediated changes in permeability to the drug and is also due to decreased binding of vancomycin to receptor molecules. 

Resistance Resistance may be caused by a change in the affinity of the DNA-dependent RNA polymerase for the drug, or by decreased permeability. 

---