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Aminoglycosides can cause inner ear toxicity which can result in sensorineural hearing loss. [19] The incidence of inner ear toxicity varies from 7 to 90%, depending on the types of antibiotics used, susceptibility of the patient to such antibiotics, and the duration of antibiotic administration. [20]
A classic example of this effect is the interaction between β-lactams, which damage the bacteria cell membrane, and aminoglycosides, which inhibit protein synthesis. [1] The damage dealt to the cell wall by β-lactams allows more aminoglycoside molecules to be taken up into the cell than would otherwise be possible, enhancing cell damage. [1]
The aminopenicillins are a group of antibiotics in the penicillin family that are structural analogs of ampicillin (which is the 2-amino derivative of benzylpenicillin, hence the name). [1] Like other penicillins and beta-lactam antibiotics , they contain a beta-lactam ring that is crucial to its antibacterial activity.
Side-effects of amikacin are similar to those of other aminoglycosides. Kidney damage and ototoxicity (which can lead to hearing loss) are the most important effects, occurring in 1–10% of users. [17] The nephro- and ototoxicity are thought to be due to aminoglycosides' tendency to accumulate in the kidneys and inner ear. [8] Diagram of the ...
Streptothricins are a group of antibiotics in the aminoglycoside class. [1] The first antibiotic in the group was isolated from Streptomyces lavendulae in 1942. [ 2 ] It was later determined to be a mixture of closely-related compounds, and is now known as nourseothricin .
Aminocyclitols are found as a component of aminoglycoside antibiotics which is also called as pseudosugars or pseudosaccharides. Aminocyclitols have chemical structures of a carbon ring with amine functional group(s). The class of aminocyclitol containing natural products can be divided by ring sizes or types of precursors.
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]
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.