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 mode of action (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:
1. 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."
2. 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.
3. Macrolides:
Macrolides exert their bateriostatic effect by binding irreversibly to the 50S subunit of bacterial ribosomes. 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, the 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.
4. Quinolones:
This broad spectrum synthetic class of antibiotic inhibits bacterial DNA replication. Representative quinolones include nalidixic acid, norfloxacin and ciprofloxacin.
5. 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. Without folic acid, the bacteria die.
6. Tetracyclines:
This class of antibiotics inhibit bacterial protein synthesis by preventing tRNA molecules from binding to the 30S ribosomal subunit. Representatives of this class include tetracycline, doxycycline and trimocycline.
* This article is for informational purposes only and is not meant to be employed in the selection and use of antibiotic treatment.
Sources
Bauman, R. (2005) Microbiology. Pearson Benjamin Cummings.
Park Talaro, K. (2008) Foundations in Microbiology. McGraw-Hill.
Published by Tami Port, MS
After completing a bachelor's degree in biology and masters degree in psychology, Tami wandered into zoo keeping, copywriting, herb farming, pharmaceutical sales, and finally teaching. She's currently an adj... View profile
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