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Index >> Bacterial Cheomotherapy >>Blocking Of Antibiotic Transport

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Bacterial Chemotherapy Part 1 Blocking of Antibiotic Transport Inactivation of Antibiotics OR Enzymatic Detoxification Bypass Mechanisms Inhibition of Protein Synthesis Stages of Translation in Protein Synthesis Initiation Process in Translation in Protein Synthesis Elongation Process in Translation in Protein Synthesis Termination Process in Translation in Protein Synthesis

Blocking Of Antibiotic Transport

	Blocking Of Antibiotic Transport - Bacteria have active transport systems designed to carry useful molecules into the cell. Certain drugs which are structurally similar to these molecules can also be transported into the bacterial cell, and are therefore used as antibiotics, Thus phosphonomycin, an analogue of phosphoenolpyuvate, can be transported into bacterial cells, and is effective as an antibiotic. Certain plasmid coded substances prevent the entry of antibiotics into the bacterial cells, thus conferring resistance to the drug.
Resistance to tetracycline, streptomycin; spectionomycin and the aminogly cosides is at least partly due to interference with drug transport. It has been suggested that resistance to tetracycline may be the result of inhibition of the normal active transport system. Tetracycline resistance is inducible, and several new proteins are produced. One of these, the Tet protein of the membrane, is a plasmid coded product studies on S. aureus indicate that tetracycline resistance is also due to the impermeability of the drug, Tetracycline resistance is transposable on several plasmids related to R100.
The transposable element for tetracycline resistance is Tn10. It can transpose between replicons at a frequency of about 10-5 per cell, per generation. It has a base sequence of about 6,500 base pairs, with an inverted repeat of 1,400 base pairs related to insertion sequence 3 (IS3) on either side. Tn 10 consists of a group of structural genes, including the tetracycline resistance genes. Its transposition is believed to be due to IS3. It was previously thought that resistance to aminoglyeoside antibiotics was due to inactivation (detoxification) mechanism.
A more detailed examination, however, shows that the resistance depends on enzymes coded by plasmids. These enzymes arc classified according to their modification mechanism (N-acetylation, O-phosphorylation Or O-nucleotidylation) and their modification Site on the aminoglycoside. The enzymes appear to be low molecular weight proteins, with the molecular weight of the monomers ranging from 17,000 to 35,000. The transport t of aminoglycosides is an active process, requiring the normal membrane-energy functions. The resistance mechanism for aminoglycoside antibiotics is presumed to be due to interference with this transport. According to one model, the antibiotic is modified by O-phosphorylation, O-nucleotidylation or N-acetylation. This results in interference or blocking of transport directly by interaction with the transport mechanism carrier.
	According to another model the rate of modification of the drug equals the s10w rate of transport, thus preventing entry of the drug into the bacterial cell. Aminoglycoside antibiotics with chemically blocked sites have been syn1hesized. They are resistant to modification by some modifying enzymes, and are therefore effective in inhibiting resistant strains.

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Bacterial Chemotherapy Part 1 Supernatant Folic Acid Antagonists Aminoalkyl Adenylates Diptheria Toxin 30S/40S Ribosomal Subunits Aminoglycosides Streptomycin Neomycin, Kanamycin and Gentamycin Tetracycines Edeine 50S/60S Ribosomal Subunit Chloramphenicol Macrolides Lincosamides Puromycin Sparsomycin Glutarimides Cycloheximide Ipeal Alkaloids Emetine

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