Mechanism of action of habekacin, a novel amino acid-containing aminoglycoside antibiotic

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Abstract
The molecular basis for activity of habekacin was studied by using Escherichia coli Q-13. EM studies revealed that numerous blebs, derived from the outer membrane, were formed on cells treated with habekacin. Cytoplasmic contents leaked into the lumina of blebs; the membrane of some enlarged blebs was disrupted. In a cell-free system, habekacin interfered with polypeptide synthesis, caused codon misreading and inhibited translocation of N-acetylphenylalanyl-tRNA from the acceptor site to the donor site on ribosomes; [3H]habekacin bound to 50S and 30S ribosomal subunits. Thus, the mechanism of action of habekacin is similar to that of 2-deoxystreptamine-containg aminoglycoside antibiotics such as dibekacin, kanamycin, gentamicin and related substances. The relationship of membrane damage to inhibition of ribosomal functions remains to be determined.

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