Protein synthesis inhibitors - SlideShare

The aminoglycosides are products of species and are represented by streptomycin, kanamycin, tobramycin and gentamicin. These antibiotics exert their activity by binding to bacterial ribosomes and preventing the initiation of protein synthesis. Aminoglycosides have been used against a wide variety of bacterial infections caused by Gram-positive and Gram-negative bacteria. Streptomycin has been used extensively as a primary drug in the treatment of tuberculosis. Gentamicin is active against many strains of Gram-positive and Gram-negative bacteria, including some strains of Pseudomonas aeruginosa. Kanamycin (a complex of three antibiotics, A, B and C) is active at low concentrations against many Gram-positive bacteria, including penicillin-resistant staphylococci. Gentamicin and Tobramycin are mainstays for treatment of Pseudomonas infections. An unfortunate side effect of aminoglycosides has tended to restrict their usage: prolonged use is known to impair kidney function and cause damage to the auditory nerves leading to deafness.

Protein Synthesis and Site of Action of Antimicrobials that Inhibit Protein Synthesis

the majority of community-acquired strains remain susceptible to the antistaphylococcal, semisynthetic penicillins and first-generation cephalosporins (), although this is changing rapidly in some countries. Agents classified as penicillinase-resistant penicillins include methicillin and nafcillin, and the isoxazoyl penicillins oxacillin, cloxacillin, dicloxacillin, and flucloxacillin. Although there is minor variation in their relative beta-lactamase stability, this does not appear to be of clinical importance. Differences in the potency of the penicillin-resistant penicillins are small, with modal minimum inhibitory concentrations (MICs) in the range of 0.125 to 0.5 ug/mL ().


Mechanism of action of antibiotics (Protein synthesis inhibitors) ..

Antibiotics: Protein Synthesis, Nucleic Acid Synthesis and Metabolism - PowerPoint PPT Presentation

: Oxazolidinones are synthetic agents, the original members of which were MAO inhibitors (). One, linezolid, is now available in some countries for the treatment of resistant staphylococcal infection (). These drugs have a novel mechanism of action on ribosomal protein synthesis, and are active against strains resistant to other classes of antibiotics (). Linezolid can be given orally as well as parenterally.


Inhibitors of the Elongation Cycle of Protein Synthesis

inhibits elongation of the protein, antibiotic/chemical agent inhibits normal nucleic acid replication examples metronidazole, binds to 30S ribosomal subunit examples tetracyclines, no glycosidic or peptide bonds form; weak cell wall result osmotic lysis, antibiotics and chemical agents affect bacterial structures or functions.

Control of Protein Synthesis - regulate the mechanisms that ..

Wilson DN (2004) Antibiotics and the inhibition of ribosome function. In: Nierhaus KH and Wilson DN (eds) Protein Synthesis and Ribosome Structure, pp. 449–527. Weinheim: Wiley‐VCH.

List of antibiotics - Wikipedia

result Leakage of cellular materials needed to sustain life., elongation of the polypeptide chain result blocks translation of mRNA into protein, Antibiotics and synthetic drugs affect bacterial structures or functions.

The following is a list of antibiotics

Streptomycin, kanamycin, gentamicin, and kasugamycin were observed to inhibit f2 phage RNA-directed protein synthesis in an system. When the reaction mixture was allowed to translate viral RNA for 5 minutes before addition of antibiotics, the synthesis was completely blocked by streptomycin or thiopeptin; but significant synthesis continued in the presence of kasugamycin, kanamycin and gentamicin. The results suggested that kasugamycin, kanamycin and gentamicin may inhibit initiation, and streptomycin may interfere with both chain initiation and elongation. Thiopeptin may affect chain elongation. The binding of fMet-tRNA to 70S ribosomes in the presence of f2 RNA was inhibited by streptomycin, kanamycin, gentamicin, and kasugamycin. The release of fMet-tRNA from the initiation complex was significantly induced by streptomycin, kanamycin, and gentamicin; but not by kasugamycin. The results indicated that the inhibition by kasugamycin of 30S initiation complex formation may result in the apparent inhibition of 70S initiation complex formation. And the apparent inhibition by streptomycin, kanamycin, and gentamicin of 70S initiation complex formation may be caused by breakdown of the complex and inhibition of ribosomal dissociation. The effects of streptomycin, kanamycin, and gentamicin were more significant with the initiation complex formed on washed 70S ribosomes than with the complex formed on unwashed 70S ribosomes. The ribosomal proteins washed out in 1 M NH4Cl protected the target sites from the antibiotic actions. The T factor- and messenger-dependent binding of Ala-tRNA to the ribosomes was significantly affected by streptomycin, but not by kanamycin, gentamicin, and kasugamycin.