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Current evidence shows that aminoglycosides do retain activity against the majority of Gram-negative clinical bacterial isolates in many parts of the world. Still, the relatively frequent occurrence of nephrotoxicity and ototoxicity during aminoglycoside treatment makes physicians reluctant to use these compounds in everyday practice.
Additionally, some antibiotics, such as aminoglycosides, may also exert undesired side effects on the neuromuscular junction. [ 7 ] Acetylcholinesterase inhibitors: Acetylcholinesterase inhibitors prevent the degradation of acetylcholine, subsequently increasing its concentration and duration of action in the neuromuscular junction. [ 8 ]
Kanamycin is in the aminoglycoside family of medications. [3] It has the weakest antibacterial capabilities of all compounds in this family when used clinically, which is partially due to its increased toxicity in comparison to other aminoglycosides. [5] It works by blocking the production of proteins that are required for bacterial survival. [3]
Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are more resistant to degradation by acetylcholinesterase, the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. This differs from acetylcholine ...
Gentamicin is a type of aminoglycoside [5] and works by disrupting the ability of the bacteria to make proteins, which typically kills the bacteria. [5] Gentamicin is naturally produced by the bacterium Micromonospora purpurea, [9] [5] was patented in 1962, approved for medical use in 1964. [10]
Resistance to aminoglycosides is conferred via numerous mechanisms: aminoglycoside-modifying enzymes and inactivation of the aminoglycosides, which is frequently seen in both gram-positive and gram-negative bacteria and is induced by nucleotidyltransferases, phosphotransferases, or aminoglycoside acetyltransferases. reduced permeability.
Macrolides, [8] clindamycin [12] and aminoglycosides [7] (with all these three having other potential mechanisms of action as well), have evidence of inhibition of ribosomal translocation. Fusidic acid prevents the turnover of elongation factor G from the ribosome.
Aminoglycoside-3'-phosphotransferase (APH(3')), also known as aminoglycoside kinase, is an enzyme that primarily catalyzes the addition of phosphate from ATP to the 3'-hydroxyl group of a 4,6-disubstituted aminoglycoside, such as kanamycin. [2]