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Twelve classes of ribosomal protection genes/proteins have been found. [35] Possible mechanisms of action of these protective proteins include: blocking tetracyclines from binding to the ribosome [36] binding to the ribosome and distorting the structure to still allow t-RNA binding while tetracycline is bound [37]
As human and bacteria both have ribosomes, streptomycin has significant side effects in humans. At low concentrations, however, streptomycin inhibits only bacterial growth. [18] Streptomycin is an antibiotic that inhibits both Gram-positive and Gram-negative bacteria, [19] and is therefore a useful broad-spectrum antibiotic.
Tetracycline, sold under various brand names, is an antibiotic in the tetracyclines family of medications, used to treat a number of infections, [3] including acne, cholera, brucellosis, plague, malaria, and syphilis. [3]
Most target bacterial functions or growth processes. [8] Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane , or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities, killing the bacteria.
There are many types of antibiotics and each class inhibits a process that is different in the pathogen from that found in the host. For example, the antibiotics chloramphenicol and tetracyclin inhibit the bacterial ribosome but not the structurally different eukaryotic ribosome, so they exhibit selective toxicity. [ 28 ]
Doxycycline is a broad-spectrum antibiotic of the tetracycline class used in the treatment of infections caused by bacteria and certain parasites. [1] It is used to treat bacterial pneumonia, acne, chlamydia infections, Lyme disease, cholera, typhus, and syphilis. [1]
Kasugamycin (Ksg) is an aminoglycoside antibiotic that was originally isolated in 1965, from Streptomyces kasugaensis, a Streptomyces strain found near the Kasuga shrine in Nara, Japan. Kasugamycin was discovered by Hamao Umezawa , who also discovered kanamycin and bleomycin , as a drug that prevent growth of a fungus causing rice blast disease .
The selectivity of the rifamycins depends on the fact that they have a very poor affinity for the analogous mammalian enzyme. Crystal structure data of the antibiotic bound to RNA polymerase indicates that rifamycin blocks synthesis by causing strong steric clashes with the growing oligonucleotide ("steric-occlusion" mechanism).