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3. ANTIBIOTIC (PROTEIN SYNTHESIS INHIBITORS)

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A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins. All of the antibiotics that target bacterial protein synthesis do so by interacting with the bacterial ribosome and inhibiting its function. The ribosome might not seem like a very good target for selective toxicity, because all cells, including our own, use ribosomes for protein synthesis.The good thing is that bacteria and eukaryotes have ribosomes that are structurally different. Bacteria have so-called 70S ribosomes and eukaryotes have 80S ribosomes. No, not '70s and '80s ribosomes, although that would be pretty entertaining. The S stands for 'Svedberg unit,' and it refers to the rate at which particles sediment down into the tube during high-speed ultracentrifugation. Basically, it tells us about the ribosome's molecular weight and shape.

70S and 80S ribosomes are different enough that antibiotics can specifically target one and not the other. Let's take a closer look at the bacterial 70S ribosome and see where some different kinds of antibiotics act on it. Remember that ribosomes are made of RNA and protein and that they have two subunits, one large and one small.

The bacterial 70S ribosome's subunits are the 50S subunit and the 30S subunit. Yes, I know, 50 + 30 = 80, not 70, but this is not a math mistake. Using the Svedberg unit to measure ribosomes means that things don't always add up perfectly, because rates of sedimentation are not additive like molecular weights are.

Before we get into the specifics of how antibiotics inhibit bacterial ribosomes, let's briefly review how ribosomes work. First, a tRNA loaded with a particular amino acid enters the ribosome at the A site. The tRNA's anticodon has to match the codon, or group of three nucleotides on the mRNA. Then, at the P site of the ribosome, a peptide bond forms between the previous amino acid and the new amino acid. Finally, the empty tRNA exits at the E site. This process repeats for the whole length of the mRNA, and the polypeptide chain continues to grow.

Publié dans : Santé & Médecine
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3. ANTIBIOTIC (PROTEIN SYNTHESIS INHIBITORS)

  1. 1. BYBY Dr.Dr. SAMINATHAN KAYAROHANAMSAMINATHAN KAYAROHANAM M.PHARM, M.B.A, PhDM.PHARM, M.B.A, PhD ANTIBIOTIC (PROTEIN SYNTHESIS INHIBITORS) 1 3
  2. 2. 2 NUM CONTENT SLIDE 1 INTRODUCTION TO PROTEIN SYNTHESIS 4 2 PROKARYOTIC AND EUKARYOTIC RIBOSOMES 5 3 GENERAL MECHANISM OF ANTIBIOTIC 6 4 CLASSIFICATION OF PROTEIN SYNTHESIS INHIBITORS 7 5 THERAPEUTIC APPLICATIONS OF TETRACYCLINES 8 6 THERAPEUTIC APPLICATIONS OF MACROLIDES 9 7 THERAPEUTIC APPLICATIONS OF LINEZOLID AND ADMINISTRATION MACROLIDE ANTIBIOTICS 10 8 PROTEIN SYNTHESIS IN RIBOSOMES 11 9 GENERAL MECHANISM OF PROTEIN SYNTHESIS INHIBITORS 12,13 10 MECHANISM OF TETRACYCLINES 14 11 MECHANISM OF AMINOGLYCOSIDES 15 12 MECHANISM OF ERYTHROMYCIN AND CLINDAMYCIN 16 13 MECHANISM OF CHLORAMPHENICOL 17 14 MECHANISM OF LINEZOLID 18 15 PHARMACOKINETICS OF SOME PROTEIN SYNTHESIS INHIBITORS AND ADVERSE EFFECTS OF TETRACYCLINE 19 16 SOME ADVERSE EFFECTS OF MACROLIDE AND AMINOGLYCOSIDES ANTIBIOTICS 20 17 DRUG INTRACTION OF PROTEIN SYNTHESIS INHIBITOR 21
  3. 3. 3 LEARNING OUTCOME 1. Able to understand the protein synthesis of prokaryotic and eukaryotic. 2. List the common protein synthesis inhibitor drug classification. 3. Abele to demonstrate the general mechanism of common protein synthesis inhibitor. 4. Able to describe the common protein synthesis inhibitor adverse effects. 5. Able to understand the therapeutic application of protein synthesis inhibitor.
  4. 4. 4 1. INTRODUCTION TO PROTEIN SYNTHESIS A protein synthesis inhibitor is a substance that stops  or slows the growth or proliferation of bacterial cells by  disrupting  the  processes  to  the  generation  of  new  proteins by targeting the bacterial ribosome. Protein  synthesis  inhibitors  usually  act  at  the  ribosome  level, taking advantage of the major differences between  prokaryotic and eukaryotic ribosome structures. Protein  synthesis  inhibitors  work  at  different  stages  of  prokaryotic mRNA translation into proteins like initiation,  elongation  (including  aminoacyl  tRNA  entry,  proofreading,  peptidyl  transfer,  and  ribosomal  translocation), and termination. Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  5. 5. 5 2. PROKARYOTIC AND EUKARYOTIC RIBOSOMES CON…Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  6. 6. 3. GENERAL MECHANISM OF ANTIBIOTIC 6 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  7. 7. 7 4. CLASSIFICATION OF PROTEIN SYNTHESIS INHIBITORS 1 2 3 4 5 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  8. 8. 5.THERAPEUTIC APPLICATIONS OF TETRACYCLINES 8 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  9. 9. 6. THERAPEUTIC APPLICATIONS OF MACROLIDES 9 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  10. 10. 10 7. THERAPEUTIC APPLICATIONS OF LINEZOLID AND ADMINISTRATION MACROLIDE ANTIBIOTICS Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  11. 11. 11 8.PROTEIN SYNTHESIS IN RIBOSOMES Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  12. 12. 9.GENERAL MECHANISM OF PROTEIN SYNTHESIS INHIBITORS Con… 12 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  13. 13. 9.GENERAL MECHANISM OF PROTEIN SYNTHESIS INHIBITORS 13 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  14. 14. Tetracyclines binds reversibly to the 30S subunit of the bacterial ribosome, thereby blocking access of the amino acyl-tRNA to the mRNA-ribosome complex at the acceptor site. By this mechanism, bacterial protein synthesis is inhibited 10. MECHANISM OF TETRACYCLINES 14 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  15. 15. 15 11. MECHANISM OF AMINOGLYCOSIDES •Susceptible gram-negative organisms allow aminoglycosides to diffuse through porin channels in their outer membranes. •oxygen-dependent system that transports the drug across the cytoplasmic membrane. •The antibiotic then binds to the 30S ribosomal subunit prior to ribosome formation. •There, it interferes with assembly of the functional ribosomal apparatus and/or can cause the 30S subunit of the completed ribosome to misread the genetic code. Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  16. 16. The macrolides bind irreversibly to a site on the 50S subunit of the bacterial ribosome, thus inhibiting the translocation steps of protein synthesis. They may also interfere at other steps, such as transpeptidation. Generally considered to be bacteriostatic, they may be bactericidal at higher doses. Their binding site is either identical or in close proximity to that for clindamycin and chloramphenicol. 12.MECHANISM OF ERYTHROMYCIN AND CLINDAMYCIN 16 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  17. 17. Chloramphenicol binds to the bacterial 50S ribosomal subunit and inhibits protein synthesis at the peptidyl transferase reaction. Because of the similarity of mammalian mitochondrial ribosomes to those of bacteria, protein synthesis in these organelles may be inhibited at high circulating chloramphenicol levels, producing bone marrow toxicity. 13. MECHANISM OF CHLORAMPHENICOL 17 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  18. 18. 18 The linezolid inhibits bacterial protein synthesis by inhibiting the formation of the 70S initiation complex. Linezolid binds to a site on the 50S subunit near the interface with the 30S subunit 14. MECHANISM OF LINEZOLID Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  19. 19. 19 15.PHARMACOKINETICS OF SOME PROTEIN SYNTHESIS INHIBITORS AND ADVERSE EFFECTS OF TETRACYCLINE. Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  20. 20. 20 16.SOME ADVERSE EFFECTS OF MACROLIDE AND AMINOGLYCOSIDES ANTIBIOTICS Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  21. 21. 21 17.DRUG INTRACTION OF PROTEIN SYNTHESIS INHIBITOR Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  22. 22. 22 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  23. 23. 23 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  24. 24. 24 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  25. 25. 25 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  26. 26. 26 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  27. 27. 27 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  28. 28. 28 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  29. 29. 29 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  30. 30. 30 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  31. 31. 31 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  32. 32. 32 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  33. 33. 33 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  34. 34. 34 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  35. 35. 35 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  36. 36. 36 TETRACYCLINE DISCOLORED TEETH Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  37. 37. 37 ACNE TREATMENT Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  38. 38. TETRACYCLINE ACNE TREATMENT 38 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  39. 39. AMINOGLYCOSIDES ANTIBIOTICS Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  40. 40. 40 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  41. 41. 41 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  42. 42. 42 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D
  43. 43. 43 Dr.K.Saminathan.M.Pharm, M.B.A, Ph.D

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