Most medically useful antibiotics interfere with either peptidogly¬can synthesis or ribosome function. Why would the cytoplasmic membrane be a poor target for antibacterial medications?
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Most medically useful antibiotics interfere with either peptidogly¬can synthesis or ribosome function. Why would the cytoplasmic membrane be a poor target for antibacterial medications?
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- Most medically useful antibiotics interfere with either peptidoglycan synthesis or ribosome function. Why would the cell membrane be a poor target for antimicrobial medication?Some antibiotics target peptidoglycan synthesis. What is amolecular growth target of an antibiotic that inhibitspeptidoglycan synthesis?For any antibiotic compounds that don’t appear to inhibit translation of proteins from the ribosome, purpose another potential mechanism whereby this class of antibiotic might be able to act (outside of cell wall/membrane formation). Explain in deatil.
- What implications does the complex hydrophobic mycobacterial cell wall have in terms of treating diseases caused by these bacteria?Antibiotics that target the cell wall have no effect on the existing peptidoglycan. So how does the antibiotic affect bacterial cells so that the cell walls become weak and the cell lyses?What kind of enzymatic activities are required to grow the peptidoglycan cell wall?
- There are many antibiotics that target the bacterial cell wall, but there are few antibiotics that target the cell membrane. Why might this be so?E. coli cells have peritrichous flagella. What does this mean?What part of a eukaryotic cell could be affected by antibiotics that target ribosomes and why?
- What are the structural reasons for therigidity that is conferred on the cell wall by the peptidoglycan structure?Antibiotic medication work by targeting specific structures and function in bacterial cells. Side effects in the patient are usually minimal, because their eukaryotic cells do not possess the same structures and characteristics as the prokaryotic pathogens. What structures or functions of the prokaryotic cell would serve as good targets for new antibiotics?The antibiotic kanamycin binds to the small ribosomal subunit of bacteria and interferes with protein synthesis, and the diphtheria toxin binds to the eukaryotic elongation factor EF2 and prevents translocation of the ribosome during protein synthesis. Suppose that an archaeobacterial infection is detected in a person. Could kanamycin and diphtheria toxin be used for treatment of the infection? Why?