Why Don’t Antibiotics Kill Our Cells?
Bacterial cells are prokaryotic; primitive cells that are very different than the eukaryotic cells that make up the human body. The MOA of antibiotics exploits the difference between these cell types so that the drugs harm bacteria without harming our cells.
MOA of Different Antibiotic Classes
The main classes of antibiotics include:
Aminoglycosides
This class of antibiotic binds to the bacterial 30S ribosomal subunit, interfering with protein synthesis.
Ribosomes are the protein factory of the cells. They are composed of two subunits, in bacteria a 30S and a larger 50S. By binding to the ribosome, aminoglycosides inhibit the translocation of tRNA during translation and leaving the bacterium unable to synthesize proteins necessary for growth. Representative aminoglycosides include kanamycin, streptomycin, gentomycin and a whole slew of other “-mycins.”
Beta-lactams
Penicillins and cephalosporins (beta-lactam antibiotics) work by interfering with interpeptide linking of peptidoglycan, a strong, structural molecule found specifically bacterial cell walls. Cell walls without intact peptidoglycan cross-links are structurally weak, prone to collapse and disintegrate when the bacteria attempts to divide. Examples of beta-lactam drugs include methicillin, amoxicillin and cefaclor.
Macrolides
Macrolides exert their bateriostatic effect by binding irreversibly to the 50S subunit of bacterial ribosomes. Ribosomes are the protein factories of the cell, and by binding to the ribosome, macrolides inhibit translocation of tRNA during translation (the production of proteins under the direction of DNA). Although the cells of humans also have ribosomes, these eukaryotic cellular protein factories differ in size and structure from the ribosomes of prokaryotes. Erythromycin, azithromycin and clarithromycin are a few examples of macrolide antibiotics.
Quinolones
This broad spectrum synthetic class of antibiotic inhibits bacterial DNA replication. Representative quinolones include nalidixic acid, norfloxacin and ciprofloxacin.
Sufonamides
These broad spectrum synthetic antibiotics were discovered by German chemist Gerhard Domagk in 1935 as the dye Prontosil. Sulfa drugs exert their action by binding irreversibly to a bacterial enzyme that produces folic acid.
Tetracyclines
This class of antibiotics inhibits bacterial protein synthesis by preventing tRNA molecules from binding to the 30S ribosomal subunit. Representatives of this class include tetracycline, doxycycline and trimocycline.
More Information on Antibiotic Mode of Action
For additional resources on how antibiotics work, see Todar’s Textbook of Bacteriology and the Science Prof Online Antibiotics Mode of Action Page containing links with details on each class of antibiotics, and the Health A to Z webpage on antibiotics.
Please note: The information in this article is not to be followed as medical advice, diagnosis or treatment. Please consult with your physician
or primary health practitioner for information regarding your own personal health and necessary treatments.
Sources
Bauman, R. (2005) Microbiology. Pearson Benjamin Cummings.
Park Talaro, K. (2008) Foundations in Microbiology. McGraw-Hill.
Image
Two bacteria of the species Staphylococcus aureus. US Agricultural Research Service, Department of Agriculture.
