“…55 Fortunately, several studies are being conducted to find drugs to protect against these undesirable effects. [57][58][59] Aminoglycoside resistance mechanisms, which in many cases coexist in the same bacterial cells, 48,60,61 include enzymatic inactivation by modifying enzymes; 5,62-64 methylation of 16S rRNA; 65,66 mutation of the 16S rRNA or ribosomal proteins to prevent binding; 65 reduced uptake that can occur by reduced inner membrane transport or modification of outer membrane's permeability; 67 export outside the cell by efflux pumps, 68 and other more rare mechanisms like active swarming or sequestration of the drug by tightly binding to an acetyltransferase of deficient activity. 69 Of all these mechanisms, the antibiotic's enzymatic inactivation mediated by aminoglycoside modifying enzymes, which catalyze the transfer of acetyl, nucleotidyl, or phosphate groups to -OH or -NH 2 positions of the aminocyclitol or the sugar moieties of the molecules, is the most prevalent in the clinical setting.…”