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MECHANISMS OF ANTIBACTERIAL
ACTIONDr. Panchumarthy ravisankar, Professor and HOD
Vignan Pharmacy College, Vadlamudi, Guntur, Andhra Pradesh, India.
INHIBITION OF BACTERIAL CELL WALL SYNTHESIS
Inhibition of bacterial cell wall synthesis leads to bacterial cell lysis and death. Agents operating in this way include penicillins, Cephalosporins
and Vancomycin. As animal cells do not have a cell wall, they are unaffected by such agents.
INHIBITION OF FOLIC ACID MEETABOLISM
Antibacterial agents act on five main targets-cell metabolism, the cell wall, the plasma membrane, protein synthesis,and nucleic acid function.
The principle of chemotherapy or the magic bullet involves the design of chemicals that show selective toxicity against bacterial cells rather
than mammalian cells.
Sulfonamides are similar in structure to para-aminobenzoic acid—a component of dihydropteroate. As a result, they can bind to the bacterial
enzyme responsible for dihydropteroate synthesis and act as an inhibitor.
Mammals synthesize tetrahydrofolate from folic acid acquired from the diet. They lack the enzyme targeted by sulfonamides. Bacteria lack
the transport mechanisms required to transport folic acid into the cell.
Trimethoprim inhibits dihydrofolate reductase—an enzyme that converts folic acid to tetrahydrofolate. It has been used in combination with
sulfamethoxazole in a strategy known as sequential blocking.
Aminoglycosides, tetracyclines, chloramphenicol, strepto-gramins, lincosamides, and macrolides inhibit protein synthesis by binding to the
bacterial ribosomes involved in the translation process.
INTERACTIONS WITH THE PLASMA MEMBRANE
Interactions with the plasma membrane: some antibacterial agents interact with the plasma membrane of bacterial cells to affect membrane
permeability. This has fatal results for the cell. Polymyxins and tyrothricin operate in this way. The peptides Valinomycin and Gramicidin
both acts on ion-conducting antibiotics (Ionophores) act on the plasma membrane and allow the uncontrolled movement of ions across the cell
membrane leading to cell death.
DISRUPTION OF PROTEIN SYNTHESIS
Disruption of protein synthesis means that essential proteins and enzymes required for the cells survival can no longer be made. Agents that
disrupt protein synthesis include the Rifamycins, Aminoglycosides, Tetracyclines, and Chloramphenicol.
INHIBITION OF NUCLEIC ACID TRANSCRIPTION AND REPLICATION
Inhibition of nucleic acid transcription and replication prevents cell division and/or the synthesis of essential proteins. Agents acting in this
way include nalidixic acid , Ciprofloxacin, Norfloxacin, Balofloxacin, Ofloxacin, Enrofloxacin, Moxifloxacin, Gatifloxacin,
Gemifloxacin, Travafloxaacin.
VIGNAN PHARMACY COLLEGE, VADLAMUDI, GUNTUR.
References
Graham L.Patrick, An introduction to Medicianl Chemistry, Oxford Universirty press Inc., New York, 2006.

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MECHANISMS OF ANTIBACTERIAL ACTION.

  • 1. MECHANISMS OF ANTIBACTERIAL ACTIONDr. Panchumarthy ravisankar, Professor and HOD Vignan Pharmacy College, Vadlamudi, Guntur, Andhra Pradesh, India. INHIBITION OF BACTERIAL CELL WALL SYNTHESIS Inhibition of bacterial cell wall synthesis leads to bacterial cell lysis and death. Agents operating in this way include penicillins, Cephalosporins and Vancomycin. As animal cells do not have a cell wall, they are unaffected by such agents. INHIBITION OF FOLIC ACID MEETABOLISM Antibacterial agents act on five main targets-cell metabolism, the cell wall, the plasma membrane, protein synthesis,and nucleic acid function. The principle of chemotherapy or the magic bullet involves the design of chemicals that show selective toxicity against bacterial cells rather than mammalian cells. Sulfonamides are similar in structure to para-aminobenzoic acid—a component of dihydropteroate. As a result, they can bind to the bacterial enzyme responsible for dihydropteroate synthesis and act as an inhibitor. Mammals synthesize tetrahydrofolate from folic acid acquired from the diet. They lack the enzyme targeted by sulfonamides. Bacteria lack the transport mechanisms required to transport folic acid into the cell. Trimethoprim inhibits dihydrofolate reductase—an enzyme that converts folic acid to tetrahydrofolate. It has been used in combination with sulfamethoxazole in a strategy known as sequential blocking. Aminoglycosides, tetracyclines, chloramphenicol, strepto-gramins, lincosamides, and macrolides inhibit protein synthesis by binding to the bacterial ribosomes involved in the translation process. INTERACTIONS WITH THE PLASMA MEMBRANE Interactions with the plasma membrane: some antibacterial agents interact with the plasma membrane of bacterial cells to affect membrane permeability. This has fatal results for the cell. Polymyxins and tyrothricin operate in this way. The peptides Valinomycin and Gramicidin both acts on ion-conducting antibiotics (Ionophores) act on the plasma membrane and allow the uncontrolled movement of ions across the cell membrane leading to cell death. DISRUPTION OF PROTEIN SYNTHESIS Disruption of protein synthesis means that essential proteins and enzymes required for the cells survival can no longer be made. Agents that disrupt protein synthesis include the Rifamycins, Aminoglycosides, Tetracyclines, and Chloramphenicol. INHIBITION OF NUCLEIC ACID TRANSCRIPTION AND REPLICATION Inhibition of nucleic acid transcription and replication prevents cell division and/or the synthesis of essential proteins. Agents acting in this way include nalidixic acid , Ciprofloxacin, Norfloxacin, Balofloxacin, Ofloxacin, Enrofloxacin, Moxifloxacin, Gatifloxacin, Gemifloxacin, Travafloxaacin. VIGNAN PHARMACY COLLEGE, VADLAMUDI, GUNTUR. References Graham L.Patrick, An introduction to Medicianl Chemistry, Oxford Universirty press Inc., New York, 2006.

Hinweis der Redaktion

  1. .,