Would an antibiotic that targets cell wall synthesis have more or less toxic side effects than one that targets the ribosome? Explain this question in detail and easy to understand
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Would an antibiotic that targets cell wall synthesis have more or less toxic side effects than one that targets the ribosome? Explain this question in detail and easy to understand
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- Most antibacterial drugs disrupt or destroy prokaryotic cellular structures or processes that are different than those of eukaryotic cells or may not even be present in eukaryotic cells. List and describe at least three prokaryotic cellular features that could be targeted to inhibit or kill a bacterial pathogen without harming its eukaryotic host.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.Some antimicrobial drugs used to treat bacterial infections disrupt the process of protein synthesis. What could these drugs target? Why would this ultimately lead to cell death?
- Most medically useful antibiotics interfere with either peptidoglycan synthesis or ribosome function. Why would the cytoplasmic membrane (in general) be a poor target for antibacterial medications?The most selectively toxic antibacterial agents are those that interfere with bacterial cell wall synthesis. This is because ________. Group of answer choices bacterial cell wall synthesis is easily inhibited whereas eukaryotic cell wall synthesis is more resistant to the actions of the drugs bacterial cell walls have a unique structure not found in eukaryotic host cells eukaryotic cells do not take up the drugs eukaryotic cells inactivate the drugs before they can do any damageExplain why drugs that effect bacterial ribosomes can be safely used in treating people.
- 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?In general, why might cell-wall inhibiting antimicrobial drugs be less effective on gram-negative bacteria compared to gram-positive bacteria? The gram-negative bacteria digest these drugs at a much higher rate than gram-positive bacteria. The mutation rate of gram-negative bacteria is much greater than that of gram-positive bacteria. The outer membrane of the gram-negative bacteria inhibits penetration of the drug. The peptidoglycan found in gram-positive bacteria is structurally different from that in gram-negative bacteria. The gram-negative bacteria do not synthesize peptidoglycan.What part of a eukaryotic cell could be affected by antibiotics that target ribosomes and why?
- Use the following statements that best describes the antibiotic mechanism for each: Statement: Targets cell wall synthesis Targets protein synthesis Targets nucleic acid synthesis Targets cell membrane Inhibits folic acid synthesis (metabolism inhibitor) E. coli plate antibiotic: Amoxicillin Cephalothin Chloramphenicol Ciprofloxicin Clindamycin Erythromycin Oxacillin Penicillin G S. aureus Other Streptomycin Tetracycline Tobramycin Trimethoprim sulfaThen there are the drugs that inhibit metabolic pathways. Describe how sulfa drugs act to prevent the bacterial cell from producing folic acid which is necessary for DNA production and thus binary fission.Antibiotic X binds to the 50S ribosomal subunit of 70S ribosomes and blocks normal ribosomal function. Which of the following is true of this drug? It would interfere with protein synthesis in bacteria, but not affect eukaryotic ribosomes. It would interfere with peptidoglycan syntheis/repair in bacteria, but not affect eukaryotes as they lack peptidoglycan. It would interfere with mRNA transcription in bacteria and in eukaryotes. It would interfere with protein synthesis in bacteria and eukaryotes. It would interfere with mRNA transcription in bacteria, but not affect eukaryotic transcription. It would interfere with peptidoglycan syntheis/repair in bacteria, as well as in eukaryotes that possess cell walls.